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For: Schmidt J, Lewandrowski K, Fernandez-del Castillo C, Mandavilli U, Compton CC, Warshaw AL, Rattner DW. Histopathologic correlates of serum amylase activity in acute experimental pancreatitis. Dig Dis Sci 1992;37:1426-33. [PMID: 1380425 DOI: 10.1007/bf01296014] [Citation(s) in RCA: 61] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]

For:	Schmidt J, Lewandrowski K, Fernandez-del Castillo C, Mandavilli U, Compton CC, Warshaw AL, Rattner DW. Histopathologic correlates of serum amylase activity in acute experimental pancreatitis. Dig Dis Sci 1992;37:1426-33. [PMID: 1380425 DOI: 10.1007/bf01296014] [Citation(s) in RCA: 61] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]

Number

Cited by Other Article(s)

Liu M, Xiao Y, Wang A. Risk factors for acute kidney injury in patients with severe acute pancreatitis: A systematic review and meta-analysis. Int J Artif Organs 2024;47:876-884. [PMID: 39506314 DOI: 10.1177/03913988241289070] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2024]

Qin A, Shi K, Tindall RR, Li J, Cheng B, Li J, Yang B, Yu Q, Zhang Y, Hong B, Kaur B, Younes M, Shen Q, Bailey-Lundberg JM, Cao Y, Ko TC. Characterization of Pancreatic Collagen-Expressing Fibroblasts in Mouse Acute Pancreatitis. GASTRO HEP ADVANCES 2024;4:100557. [PMID: 39866719 PMCID: PMC11761323 DOI: 10.1016/j.gastha.2024.09.012] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 01/03/2024] [Accepted: 09/16/2024] [Indexed: 01/28/2025]

Tindall RR, Yang Y, Hernandez I, Qin A, Li J, Zhang Y, Gomez TH, Younes M, Shen Q, Bailey-Lundberg JM, Zhao Z, Kraushaar D, Castro P, Cao Y, Zheng WJ, Ko TC. Aging- and alcohol-associated spatial transcriptomic signature in mouse acute pancreatitis reveals heterogeneity of inflammation and potential pathogenic factors. J Mol Med (Berl) 2024;102:1051-1061. [PMID: 38940937 PMCID: PMC11269349 DOI: 10.1007/s00109-024-02460-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2023] [Revised: 03/15/2024] [Accepted: 06/07/2024] [Indexed: 06/29/2024]

Abstract

The rapidly aging population is consuming more alcohol, leading to increased alcohol-associated acute pancreatitis (AAP) with high mortality. However, the mechanisms remain undefined, and currently there are no effective therapies available. This study aims to elucidate aging- and alcohol-associated spatial transcriptomic signature by establishing an aging AAP mouse model and applying Visium spatial transcriptomics for understanding of the mechanisms in the context of the pancreatic tissue. Upon alcohol diet feeding and caerulein treatment, aging mice (18 months) developed significantly more severe AAP with 5.0-fold increase of injury score and 2.4-fold increase of amylase compared to young mice (3 months). Via Visium spatial transcriptomics, eight distinct tissue clusters were revealed from aggregated transcriptomes of aging and young AAP mice: five acinar, two stromal, and one islet, which were then merged into three clusters: acinar, stromal, and islet for the comparative analysis. Compared to young AAP mice, > 1300 differentially expressed genes (DEGs) and approximately 3000 differentially regulated pathways were identified in aging AAP mice. The top five DEGs upregulated in aging AAP mice include Mmp8, Ppbp, Serpina3m, Cxcl13, and Hamp with heterogeneous distributions among the clusters. Taken together, this study demonstrates spatial heterogeneity of inflammatory processes in aging AAP mice, offering novel insights into the mechanisms and potential drivers for AAP development. KEY MESSAGES: Mechanisms regarding high mortality of AAP in aging remain undefined. An aging AAP mouse model was developed recapturing clinical exhibition in humans. Spatial transcriptomics identified contrasted DEGs in aging vs. young AAP mice. Top five DEGs were Mmp8, Ppbp, Serpina3m, Cxcl13, and Hamp in aging vs. young AAP mice. Our findings shed insights for identification of molecular drivers in aging AAP.

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Yin J, Huang Y, Wang K, Zhong Q, Liu Y, Ji Z, Liao Y, Ma Z, Bei W, Wang W. Ginseng extract improves pancreatic islet injury and promotes β-cell regeneration in T2DM mice. Front Pharmacol 2024;15:1407200. [PMID: 38989151 PMCID: PMC11234855 DOI: 10.3389/fphar.2024.1407200] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2024] [Accepted: 06/03/2024] [Indexed: 07/12/2024] Open

Abstract

Introduction

Panax ginseng C. A. Mey. (Araliaceae; Ginseng Radix et Rhizoma), a traditional plant commonly utilized in Eastern Asia, has demonstrated efficacy in treating neuro-damaging diseases and diabetes mellitus. However, its precise roles and mechanism in alleviating type 2 diabetes mellitus (T2DM) need further study. The objective of this study is to explore the pharmacological effects of ginseng extract and elucidate its potential mechanisms in protecting islets and promoting β-cell regeneration.

Methods

The T2DM mouse model was induced through streptozotocin combined with a high-fat diet. Two batches of mice were sacrificed on the 7th and 28th days following ginseng extract administration. Body weight, fasting blood glucose levels, and glucose tolerance were detected. Morphological changes in the pancreatic islets were examined via H & E staining. Levels of serum insulin, glucagon, GLP-1, and inflammatory factors were measured using ELISA. The ability of ginseng extract to promote pancreatic islet β-cell regeneration was evaluated through insulin & PCNA double immunofluorescence staining. Furthermore, the mechanism behind β-cells regeneration was explored through insulin & glucagon double immunofluorescence staining, accompanied by immunohistochemical staining and western blot analyses.

Results and Discussion

The present research revealed that ginseng extract alleviates symptoms of T2DM in mice, including decreased blood glucose levels and improved glucose tolerance. Serum levels of insulin, GLP-1, and IL-10 increased following the administration of ginseng extract, while levels of glucagon, TNF-α, and IL-1β decreased. Ginseng extract preserved normal islet morphology, increased nascent β-cell population, and inhibited inflammatory infiltration within the islets, moreover, it decreased α-cell proportion while increasing β-cell proportion. Mechanistically, ginseng extract might inhibit ARX and MAFB expressions, increase MAFA level to aid in α-cell to β-cell transformation, and activate AKT-FOXM1/cyclin D2 to enhance β-cell proliferation. Our study suggests that ginseng extract may be a promising therapy in treating T2DM, especially in those with islet injury.

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Affiliation(s)

Jianying Yin Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Yuanfeng Huang Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Ke Wang Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Qin Zhong Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Yuan Liu Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Zirui Ji Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Yiwen Liao Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Zhiyuan Ma Baishan Institute of Science and Technology, Baishan, Jilin, China
Weijian Bei Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
Weixuan Wang Traditional Chinese Medicine Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China Guangdong Provincial Research Center of Integration of Traditional Chinese Medicine and Western Medicine in Metabolic Diseases, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China

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Fukuda Y, Mori K, Okada H, Tomita H, Suzuki K, Takada C, Kamidani R, Kawasaki Y, Fukuda H, Minamiyama T, Nishio A, Shimada T, Kuroda A, Uchida A, Kitagawa Y, Fukuta T, Miyake T, Yoshida T, Suzuki A, Tetsuka N, Yoshida S, Ogura S. Decreased neutrophil counts prolong inflammation in acute pancreatitis and cause inflammation spillover to distant organs. Pancreatology 2023;23:911-918. [PMID: 37981522 DOI: 10.1016/j.pan.2023.10.020] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/31/2023] [Revised: 07/18/2023] [Accepted: 10/26/2023] [Indexed: 11/21/2023]

Affiliation(s)

Yohei Fukuda Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Kosuke Mori Department of Tumor Pathology, Gifu University Graduate School of Medicine, Japan
Hideshi Okada Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan; Center for One Medicine Innovative Translational Research, Gifu University Institute for Advanced Study, Japan.
Hiroyuki Tomita Department of Tumor Pathology, Gifu University Graduate School of Medicine, Japan; Center for One Medicine Innovative Translational Research, Gifu University Institute for Advanced Study, Japan.
Kodai Suzuki Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Chihiro Takada Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Ryo Kamidani Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Yuki Kawasaki Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Hirotsugu Fukuda Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Toru Minamiyama Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Ayane Nishio Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Takuto Shimada Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Ayumi Kuroda Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Akihiro Uchida Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Yuichiro Kitagawa Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Tetsuya Fukuta Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Takahito Miyake Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Takahiro Yoshida Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan
Akio Suzuki Department of Pharmacy, Gifu University Hospital, Japan
Nobuyuki Tetsuka Department of Infection Control, Gifu University Graduate School of Medicine, Japan
Shozo Yoshida Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan; Abuse Prevention Emergency Medicine, Gifu University Graduate School of Medicine, Gifu, Japan
Shinji Ogura Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Japan

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Smoday IM, Petrovic I, Kalogjera L, Vranes H, Zizek H, Krezic I, Gojkovic S, Skorak I, Hriberski K, Brizic I, Kubat M, Strbe S, Barisic I, Sola M, Lovric E, Lozic M, Boban Blagaic A, Skrtic A, Seiwerth S, Sikiric P. Therapy Effect of the Stable Gastric Pentadecapeptide BPC 157 on Acute Pancreatitis as Vascular Failure-Induced Severe Peripheral and Central Syndrome in Rats. Biomedicines 2022;10:1299. [PMID: 35740321 PMCID: PMC9220115 DOI: 10.3390/biomedicines10061299] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/16/2022] [Revised: 05/24/2022] [Accepted: 05/27/2022] [Indexed: 12/15/2022] Open

Abstract

We revealed the therapy effect of the stable gastric pentadecapeptide BPC 157 (10 μg/kg, 10 ng/kg ig or po) with specific activation of the collateral rescuing pathways, the azygos vein, on bile duct ligation in particular, and acute pancreatitis as local disturbances (i.e., improved gross and microscopy presentation, decreased amylase level). Additionally, we revealed the therapy's effect on the acute pancreatitis as vascular failure and multiorgan failure, both peripherally and centrally following "occlusion-like" syndrome, major intoxication (alcohol, lithium), maintained severe intra-abdominal hypertension, and myocardial infarction, or occlusion syndrome, and major vessel occlusion. The application-sacrifice periods were ligation times of 0-30 min, 0-5 h, 0-24 h (cured periods, early regimen) and 4.30 h-5 h, 5 h-24 h (cured periods, delayed regimen). Otherwise, bile duct-ligated rats commonly presented intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, gross brain swelling, hemorrhage and lesions, heart dysfunction, lung lesions, liver and kidney failure, gastrointestinal lesions, and severe arterial and venous thrombosis, peripherally and centrally. Unless antagonized with the key effect of BPC 157 regimens, reversal of the inferior caval and superior mesenteric vein congestion and reversal of the failed azygos vein activated azygos vein-recruited direct delivery to rescue the inferior-superior caval vein pathway; these were all antecedent to acute pancreatitis major lesions (i.e., acinar, fat necrosis, hemorrhage). These lesions appeared in the later period, but were markedly attenuated/eliminated (i.e., hemorrhage) in BPC 157-treated rats. To summarize, while the innate vicious cycle may be peripheral (bile duct ligation), or central (rapidly developed brain disturbances), or peripheral and central, BPC 157 resolved acute pancreatitis and its adjacent syndrome.

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Affiliation(s)

Ivan Maria Smoday Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Igor Petrovic Department of Surgery, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia;
Luka Kalogjera Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Hrvoje Vranes Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Helena Zizek Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Ivan Krezic Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Slaven Gojkovic Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Ivan Skorak Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Klaudija Hriberski Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Ivan Brizic Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Milovan Kubat Department of Forensic Medicine and Criminology, School of Medicne, 10000 Zagreb, Croatia;
Sanja Strbe Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Ivan Barisic Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Marija Sola Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Eva Lovric Department of Pathology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (E.L.); (S.S.)
Marin Lozic Department of Pediatric and Preventive Dentistry, School of Dental Medicine, University of Zagreb, 10000 Zagreb, Croatia;
Alenka Boban Blagaic Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)
Anita Skrtic Department of Pathology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (E.L.); (S.S.)
Sven Seiwerth Department of Pathology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (E.L.); (S.S.)
Predrag Sikiric Department of Pharmacology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia; (I.M.S.); (L.K.); (H.V.); (H.Z.); (I.K.); (S.G.); (I.S.); (K.H.); (I.B.); (S.S.); (I.B.); (M.S.); (A.B.B.)

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Alves FDAV, Oliveira LDLS, Salomão NG, Provance DW, Basilio-de-Oliveira CA, Basílio-de-Oliveira R, Moragas LJ, de Carvalho JJ, Mohana-Borges R, Rabelo K, Paes MV. Cytokines and inflammatory mediators: Markers involved in interstitial damage to the pancreas in two dengue fever cases associated with acute pancreatitis. PLoS One 2022;17:e0262785. [PMID: 35041718 PMCID: PMC8765625 DOI: 10.1371/journal.pone.0262785] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2021] [Accepted: 01/04/2022] [Indexed: 12/15/2022] Open

Zhang Q, Zhou J, Zhou J, Fang RH, Gao W, Zhang L. Lure-and-kill macrophage nanoparticles alleviate the severity of experimental acute pancreatitis. Nat Commun 2021;12:4136. [PMID: 34230486 PMCID: PMC8260623 DOI: 10.1038/s41467-021-24447-4] [Citation(s) in RCA: 44] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2021] [Accepted: 06/17/2021] [Indexed: 02/08/2023] Open

Guo Y, Hu W, Wang X, Li C, Cui T, Liu R, He J, Yin C. PSD-95 protects the pancreas against pathological damage through p38 MAPK signaling pathway in acute pancreatitis. Exp Biol Med (Maywood) 2021;246:1473-1482. [PMID: 33794695 DOI: 10.1177/15353702211003293] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open

Abstract

Acute pancreatitis is one of the leading causes of gastrointestinal disorder-related hospitalizations, yet its pathogenesis remains to be fully elucidated. Postsynaptic density protein-95 (PSD-95) is closely associated with tissue inflammation and injury. We aimed to investigate the expression of PSD-95 in pancreatic acinar cells, and its function in regulating the inflammatory response and pancreatic pathological damage in acute pancreatitis. A mouse model of edematous acute pancreatitis was induced with caerulein and lipopolysaccharide in C57BL/6 mice. Tat-N-dimer was injected to inhibit the PSD-95 activity separately, or simultaneously with SB203580, inhibitor of p38 MAPK phosphorylation. Rat pancreatic acinar cells AR42J were cultured with 1 μM caerulein to build a cell model of acute pancreatitis. PSD-95-knockdown and negative control cell lines were constructed by lentiviral transfection of AR42J cells. Paraffin-embedded pancreatic tissue samples were processed for routine HE staining to evaluate the pathological changes of human and mouse pancreatic tissues. Serum amylase and inflammatory cytokine levels were detected with specific ELISA kits. Immunofluorescence, immunohistochemical, Western-blot, and qRT-PCR were used to detect the expression levels of PSD-95, p38, and phosphorylated p38. Our findings showed that PSD-95 is expressed in the pancreatic tissues of humans, C57BL/6 mice, and AR42J cells, primarily in the cytoplasm. PSD-95 expression increased at 2 h, reaching the peak at 6 h in mice and 12 h in AR42J cells. IL-6, IL-8, and TNF-α increased within 2 h of disease induction. The pancreatic histopathologic score was greater in the PSD-95 inhibition group compared with the control (P < 0.05), while it was lesser when phosphorylation of p38 MAPK was inhibited compared with the PSD-95 inhibition group (P < 0.05). Moreover, phosphorylation of p38 MAPK increased statistically after PSD-95 knocked-down. In conclusion, PSD-95 effectively influences the pathological damage of the pancreas in acute pancreatitis by affecting the phosphorylation of p38 MAPK.

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Bansod S, Chilvery S, Saifi MA, Das TJ, Tag H, Godugu C. Borneol protects against cerulein-induced oxidative stress and inflammation in acute pancreatitis mice model. ENVIRONMENTAL TOXICOLOGY 2021;36:530-539. [PMID: 33166053 DOI: 10.1002/tox.23058] [Citation(s) in RCA: 20] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/07/2019] [Revised: 09/09/2020] [Accepted: 10/22/2020] [Indexed: 06/11/2023]

Yang B, Davis JM, Gomez TH, Younes M, Zhao X, Shen Q, Wang R, Ko TC, Cao Y. Characteristic pancreatic and splenic immune cell infiltration patterns in mouse acute pancreatitis. Cell Biosci 2021;11:28. [PMID: 33531047 PMCID: PMC7852096 DOI: 10.1186/s13578-021-00544-1] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/17/2020] [Accepted: 01/21/2021] [Indexed: 12/22/2022] Open

Bansod S, Godugu C. Nimbolide ameliorates pancreatic inflammation and apoptosis by modulating NF-κB/SIRT1 and apoptosis signaling in acute pancreatitis model. Int Immunopharmacol 2020;90:107246. [PMID: 33310297 DOI: 10.1016/j.intimp.2020.107246] [Citation(s) in RCA: 22] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/16/2020] [Revised: 11/25/2020] [Accepted: 11/25/2020] [Indexed: 12/12/2022]

The protective effect of betacellulin against acute pancreatitis is ERBB4 dependent. J Gastroenterol 2020;55:317-329. [PMID: 31456099 DOI: 10.1007/s00535-019-01613-6] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/07/2019] [Accepted: 08/15/2019] [Indexed: 02/07/2023]

Kim YS, Chang JH, Kim TH, Kim CW, Kim JK, Han SW. Prolonged hyperamylasemia in patients with acute pancreatitis is associated with recurrence of acute pancreatitis. Medicine (Baltimore) 2020;99:e18861. [PMID: 32011507 PMCID: PMC7220070 DOI: 10.1097/md.0000000000018861] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open

Amiti, Tamizhselvi R, Manickam V. Menadione (vitamin K3) inhibits hydrogen sulfide and substance P via NF-кB pathway in caerulein-induced acute pancreatitis and associated lung injury in mice. Pancreatology 2019;19:266-273. [PMID: 30685119 DOI: 10.1016/j.pan.2019.01.012] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/07/2018] [Revised: 01/11/2019] [Accepted: 01/16/2019] [Indexed: 12/11/2022]

Wang B, Hu C, Mei Y, Bao J, Ding S, Liu X, Mei Q, Xu J. Resolvin D1 Resolve Inflammation in Experimental Acute Pancreatitis by Restoring Autophagic Flux. Dig Dis Sci 2018;63:3359-3366. [PMID: 29974378 DOI: 10.1007/s10620-018-5191-4] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/29/2017] [Accepted: 06/28/2018] [Indexed: 12/19/2022]

Emodin Attenuates Autophagy Response to Protect the Pancreas From Acute Pancreatitis Failure. Pancreas 2018;47:892-897. [PMID: 29912852 DOI: 10.1097/mpa.0000000000001080] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]

Suppression of inducible nitric oxide synthase and tumor necrosis factor-alpha level by lycopene is comparable to methylprednisolone in acute pancreatitis. Dig Liver Dis 2018;50:601-607. [PMID: 29439880 DOI: 10.1016/j.dld.2018.01.131] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/02/2017] [Revised: 01/17/2018] [Accepted: 01/17/2018] [Indexed: 12/11/2022]

Anti-inflammatory and Antioxidant Effects of Captopril Compared to Methylprednisolone in L-Arginine-Induced Acute Pancreatitis. Dig Dis Sci 2018;63:1497-1505. [PMID: 29594979 DOI: 10.1007/s10620-018-5036-1] [Citation(s) in RCA: 23] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/22/2017] [Accepted: 03/22/2018] [Indexed: 12/12/2022]

Protective Effect of Scopoletin Against Cerulein-Induced Acute Pancreatitis and Associated Lung Injury in Mice. Pancreas 2018;47:577-585. [PMID: 29595543 DOI: 10.1097/mpa.0000000000001034] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]

Li L, Sun Z, Xu C, Wu J, Liu G, Cui H, Chen H. Adenovirus-mediated overexpression of sST2 attenuates cardiac injury in the rat with severe acute pancreatitis. Life Sci 2018;202:167-174. [PMID: 29653119 DOI: 10.1016/j.lfs.2018.04.008] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2017] [Revised: 03/29/2018] [Accepted: 04/08/2018] [Indexed: 12/12/2022]

Abstract

AIMS

Severe acute pancreatitis (SAP) is a serious disease associated with systematic inflammation and multiple organs dysfunction. Soluble ST2 (sST2), a member of the Toll interleukin (IL)-1 receptor (TIR) superfamily, has been demonstrated to exert immune-regulatory and anti-inflammatory properties in several inflammation-related diseases. In this study, we investigated whether transfer of sST2 gene by adenovirus vector could attenuate sodium taurocholate-induced SAP and associated cardiac injury.

MAIN METHODS

A rat model of SAP was induced by retrograde injection of 5% sodium taurocholate (1 ml/kg) into the biliopancreatic duct. Rats in the treatment groups were intravenously injected with adenovirus expressing sST2 (Ad-sST2, 1 × 10⁹ particles/rat) or green fluorescent protein (Ad-GFP) via the tail vein 48 h before SAP induction. Histological changes in the pancreatic and heart tissues, and parameters for evaluating SAP and associated cardiac injury were determined at 24 h after SAP.

KEY FINDINGS

Sodium taurocholate induced obvious pathological changes in pancreas and elevated serum levels of amylase and lipase. Furthermore, SAP animals exhibited significant cardiac impairment, evidenced by decreased cardiac function, increased myocardial apoptosis and cardiac-related enzymes including creatine kinase isoenzyme, lactate dehydrogenase, and Troponin T. Administration of Ad-sST2 markedly improved the structure of pancreas and heart tissues, and reversed the alterations in serum amylase, lipase and cardiac-related enzymes. In addition, Ad-sST2 treatment downregulated pro-inflammatory cytokines production, demonstrating the anti-inflammatory property of sST2.

SIGNIFICANCE

Our results suggest that administration of Ad-sST2 significantly attenuated the severity of SAP and associated cardiac damage, and the cardioprotective effect is associated with its anti-inflammatory action.

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Liao D, Qian B, Zhang Y, Wu K, Xu M. Inhibition of 5-lipoxygenase represses neutrophils activation and activates apoptosis in pancreatic tissues during acute necrotizing pancreatitis. Biochem Biophys Res Commun 2018;498:79-85. [PMID: 29421656 DOI: 10.1016/j.bbrc.2018.02.026] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2018] [Accepted: 02/03/2018] [Indexed: 11/29/2022]

Ye X, Ding J, Chen Y, Dong J. Adenovirus-mediated artificial miRNA targetting fibrinogen-like protein 2 attenuates the severity of acute pancreatitis in mice. Biosci Rep 2017;37:BSR20170964. [PMID: 29054965 PMCID: PMC5700271 DOI: 10.1042/bsr20170964] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2017] [Revised: 12/10/2017] [Accepted: 10/17/2017] [Indexed: 12/19/2022] Open

Iyer S, Park MJ, Moons D, Kwan R, Liao J, Liu L, Omary MB. Clusterin and Pycr1 alterations associate with strain and model differences in susceptibility to experimental pancreatitis. Biochem Biophys Res Commun 2017;482:1346-1352. [PMID: 27939882 PMCID: PMC5240812 DOI: 10.1016/j.bbrc.2016.12.039] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/24/2016] [Accepted: 12/06/2016] [Indexed: 01/15/2023]

Abstract

Acute pancreatitis has several underlying etiologies, and results in consequences ranging from mild to complex multi-organ failure. The wide range of pathology suggests a genetic predisposition for progression. We compared the susceptibility to acute pancreatitis in BALB/c and FVB/N mice, coupled with proteomic analysis, in order to identify potential protein associations with pancreatitis progression.

METHODS

Pancreatitis was induced in BALB/c and FVB/N mice by administration of cerulein or feeding a choline-deficient, ethionine-supplemented (CDE) diet. Histology and changes in serum amylase were examined. Proteome profiling in cerulein-treated mice was performed using 2-dimensional differential in gel electrophoresis (2D-DIGE) followed by mass spectrometry analysis and biochemical validation.

RESULTS

Male and female FVB/N mice manifested more severe cerulein-induced pancreatitis as compared with BALB/c mice, but both strains were similarly susceptible to CDE-induced pancreatitis. Few of the 2D-DIGE alterations were validated by immunoblotting. Clusterin was markedly up-regulated after cerulein-induced pancreatitis in FVB/N but less-so in BALB/c mice. Pyrroline-5-carboxylate reductase (Pycr1), an enzyme involved in proline biosynthesis, had higher basal levels in FVB/N male and female mouse pancreata compared with BALB/c pancreata, and was relatively more resistant to degradation in FVB/N pancreata. However, serum and pancreas tissue proline levels were similar in the two strains.

CONCLUSION

FVB/N is more susceptible than BALB/c mice to cerulein-induced but not CDE-induced pancreatitis. Most of the 2D-DIGE alterations in the two strains likely relate to posttranslational modifications rather than protein level differences. Clusterin levels increase dramatically in association with pancreatitis severity, while Pycr1 is higher in FVB/N versus BALB/c pancreata basally and after induction of pancreatitis. Changes in proline metabolism may represent a novel potential genetic modifier in the context of pancreatitis.

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Osteomyelitis: A rare complication of pancreatitis and PPP-syndrome. Joint Bone Spine 2015;83:221-4. [PMID: 26471414 DOI: 10.1016/j.jbspin.2015.05.005] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2015] [Accepted: 05/28/2015] [Indexed: 12/16/2022]

Hu YY, Zhou CH, Dou WH, Tang W, Hu CY, Hu DM, Feng H, Wang JZ, Qian MJ, Cheng GL, Wang SF. Improved autophagic flux is correlated with mTOR activation in the later recovery stage of experimental acute pancreatitis. Pancreatology 2015;15:470-477. [PMID: 26164831 DOI: 10.1016/j.pan.2015.06.004] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/24/2015] [Revised: 05/20/2015] [Accepted: 06/15/2015] [Indexed: 12/11/2022]

Overexpression of Fas and FasL is associated with infectious complications and severity of experimental severe acute pancreatitis by promoting apoptosis of lymphocytes. Inflammation 2015;37:1202-12. [PMID: 24566874 PMCID: PMC4077252 DOI: 10.1007/s10753-014-9847-8] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]

MicroRNAs in mesenteric lymph and plasma during acute pancreatitis. Ann Surg 2015;260:341-7. [PMID: 24509209 DOI: 10.1097/sla.0000000000000447] [Citation(s) in RCA: 46] [Impact Index Per Article: 4.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

Potential Effects of Calcium Binding Protein S100A12 on Severity Evaluation and Curative Effect of Severe Acute Pancreatitis. Inflammation 2014;38:290-7. [DOI: 10.1007/s10753-014-0032-x] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]

Jacob TG, Raghav R, Kumar A, Garg PK, Roy TS. Duration of injury correlates with necrosis in caerulein-induced experimental acute pancreatitis: implications for pathophysiology. Int J Exp Pathol 2014;95:199-208. [PMID: 24761825 DOI: 10.1111/iep.12081] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/18/2013] [Accepted: 03/03/2014] [Indexed: 12/17/2022] Open

Ozaki N, Fukuchi Y, Tomiyoshi SR, Uehara H, Ida S, Wang J, Araki K, Sibilia M, Baba H, Yamamura KI, Ohmuraya M. Autophagy regulation in pancreatic acinar cells is independent of epidermal growth factor receptor signaling. Biochem Biophys Res Commun 2014;446:224-30. [DOI: 10.1016/j.bbrc.2014.02.111] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/18/2014] [Accepted: 02/21/2014] [Indexed: 01/20/2023]

Ang AD, Rivers-Auty J, Hegde A, Ishii I, Bhatia M. The effect of CSE gene deletion in caerulein-induced acute pancreatitis in the mouse. Am J Physiol Gastrointest Liver Physiol 2013;305:G712-G721. [PMID: 24008358 DOI: 10.1152/ajpgi.00044.2013] [Citation(s) in RCA: 42] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]

Akyazi I, Eraslan E, Gülçubuk A, Ekiz EE, Çırakli ZL, Haktanir D, Bala DA, Özkurt M, Matur E, Özcan M. Long-term aspirin pretreatment in the prevention of cerulein-induced acute pancreatitis in rats. World J Gastroenterol 2013;19:2894-2903. [PMID: 23704822 PMCID: PMC3660814 DOI: 10.3748/wjg.v19.i19.2894] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/14/2012] [Revised: 01/15/2013] [Accepted: 02/06/2013] [Indexed: 02/06/2023] Open

Abstract

AIM: To investigate the effects of long term pretreatment with low-, medium- and high-dose aspirin (acetylsalicylic acid, ASA) on a model of acute pancreatitis (AP) induced in rats.

METHODS: Forty male Wistar rats were used. Three experimental groups, each consisting of eight animals, received low- (5 mg/kg per day), medium- (150 mg/kg per day) and high-dose (350 mg/kg per day) ASA in supplemented pellet chow for 100 d. Eight animals, serving as the AP-control group, and another eight, serving as reference value (RV) group, were fed with standard pellet chow for the same period. After pretreatment, AP was induced in the experimental animals by intraperitoneal administration of cerulein (2 × 50 μg/kg), while the RV group received saline in the same way. Twelve hours after the second injection, the animals were sacrificed. Pancreatic tissue and plasma samples were collected. One part of the collected pancreatic tissues was used for histopathological evaluation, and the remaining portion was homogenized. Cytokine levels [tumor necrosis factor, interleukin (IL)-1β, IL-6], hemogram parameters, biochemical parameters (amylase and lipase), nuclear factor-κB, aspirin triggered lipoxins and parameters related to the antioxidant system (malondialdehyde, nitric oxide, hemeoxygenase-1, catalase and superoxide dismutase) were measured.

RESULTS: Cerulein administration induced mild pancreatitis, characterized by interstitial edema (total histopathological score of 5.88 ± 0.44 vs 0.25 ± 0.16, P < 0.001). Subsequent pancreatic tissue damage resulted in an increase in amylase (2829.71 ± 772.48 vs 984.57 ± 49.22 U/L, P = 0.001) and lipase (110.14 ± 75.84 U/L vs 4.71 ± 0.78 U/L, P < 0.001) in plasma, and leucocytes (6.89 ± 0.48 vs 4.36 ± 0.23, P = 0.001) in peripheral blood. Cytokines, IL-1β (18.81 ± 2.55 pg/μg vs 6.65 ± 0.24 pg/μg, P = 0.002) and IL-6 (14.62 ± 1.98 pg/μg vs 9.09 ± 1.36 pg/μg, P = 0.04) in pancreatic tissue also increased. Aspirin pretreatment reduced the increase in the aforementioned parameters to a certain degree and partially improved the histopathological alterations caused by cerulein. No evidence of side effects related to chronic ASA administration (e.g., inflammation or bleeding) was observed in the gastrointestinal tract in macroscopic and histopathological examination.

CONCLUSION: Long term ASA pretreatment could prevent and/or ameliorate certain hematological, serological and histological alterations caused by cerulein-induced AP.

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Ye XH, Chen TZ, Huai JP, Lu GR, Zhuge XJ, Chen RP, Chen WJ, Wang C, Huang ZM. Correlation of fibrinogen-like protein 2 with progression of acute pancreatitis in rats. World J Gastroenterol 2013;19:2492-2500. [PMID: 23674850 PMCID: PMC3646139 DOI: 10.3748/wjg.v19.i16.2492] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/17/2012] [Revised: 11/09/2012] [Accepted: 01/05/2013] [Indexed: 02/06/2023] Open

Abstract

AIM

To examine fibrinogen-like protein 2 (fgl2) expression during taurocholate-induced acute pancreatitis progression in rats and its correlation with pancreatic injury severity.

METHODS

Forty-eight male Sprague-Dawley rats were randomly divided into the severe acute pancreatitis (SAP) group (n = 24) and the sham operation (SO) group (n = 24). Sodium taurocholate (4% at doses of 1 mL/kg body weight) was retrogradely injected into the biliopancreatic ducts of the rats to induce SAP. Pancreatic tissues were prepared immediately after sacrifice. At the time of sacrifice, blood was obtained for determination of serum amylase activity and isolation of peripheral blood mononuclear cells (PBMCs). Pancreatic tissue specimens were obtained for routine light microscopy including hematoxylin and eosin staining, and the severity of pancreatic injury was evaluated 1, 4 and 8 h after induction. Expression of fgl2 mRNA was measured in the pancreas and PBMCs using reverse transcription polymerase chain reaction. Expression of fgl2 protein was evaluated in pancreatic tissues using Western blotting and immunohistochemical staining. Masson staining was also performed to observe microthrombosis.

RESULTS

At each time point, levels of fgl2 mRNAs in pancreatic tissues and PBMCs were higher (P < 0.05) in the SAP group than in the SO group. For pancreatic tissue in SAP vs SO, the levels were: after 1 h, 3.911 ± 1.277 vs 1.000 ± 0.673; after 4 h, 9.850 ± 3.095 vs 1.136 ± 0.609; and after 8 h, 12.870 ± 3.046 vs 1.177 ± 0.458. For PBMCs in SAP vs SO, the levels were: after 1 h, 2.678 ± 1.509 vs 1.000 ± 0.965; after 4 h, 6.922 ± 1.984 vs 1.051 ± 0.781; and after 8 h, 13.533 ± 6.575 vs 1.306 ± 1.179. Levels of fgl2 protein expression as determined by Western blotting and immunohistochemical staining were markedly up-regulated (P < 0.001) in the SAP group compared with those in the SO group. For Western blotting in SAP vs SO, the results were: after 1 h, 2.183 ± 0.115 vs 1.110 ± 0.158; after 4 h, 2.697 ± 0.090 vs 0.947 ± 0.361; and after 8 h, 3.258 ± 0.094 vs 1.208 ± 0.082. For immunohistochemical staining in SAP vs SO, the results were: after 1 h, 1.793 ± 0.463 vs 0.808 ± 0.252; after 4 h, 4.535 ± 0.550 vs 0.871 ± 0.318; and after 8 h, 6.071 ± 0.941 vs 1.020 ± 0.406. Moreover, we observed a positive correlation in the pancreas (r = 0.852, P < 0.001) and PBMCs (r = 0.735, P < 0.001) between fgl2 expression and the severity of pancreatic injury. Masson staining showed that microthrombosis (%) in rats with SAP was increased (P < 0.001) compared with that in the SO group and it was closely correlated with fgl2 expression in the pancreas (r = 0.842, P < 0.001). For Masson staining in SAP vs SO, the results were: after 1 h, 26.880 ± 9.031 vs 8.630 ± 3.739; after 4 h, 53.750 ± 19.039 vs 8.500 ± 4.472; and after 8 h, 80.250 ± 12.915 vs 10.630 ± 7.003.

CONCLUSION

Microthrombosis due to fgl2 overexpression contributes to pancreatic impairment in rats with SAP, and fgl2 level may serve as a biomarker during early stages of disease.

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Noggin attenuates cerulein-induced acute pancreatitis and impaired autophagy. Pancreas 2013;42:301-7. [PMID: 22850625 PMCID: PMC3894737 DOI: 10.1097/mpa.0b013e31825b9f2c] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]

Mittal A, Hickey AJR, Chai CC, Loveday BPT, Thompson N, Dare A, Delahunt B, Cooper GJS, Windsor JA, Phillips ARJ. Early organ-specific mitochondrial dysfunction of jejunum and lung found in rats with experimental acute pancreatitis. HPB (Oxford) 2011;13:332-41. [PMID: 21492333 PMCID: PMC3093645 DOI: 10.1111/j.1477-2574.2010.00290.x] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]

The redox status of experimental hemorrhagic shock as measured by cyclic voltammetry. Shock 2010;33:460-6. [PMID: 19789466 DOI: 10.1097/shk.0b013e3181c0ea12] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]

The Potential Effect of Proteasome Inhibitor PS-341 on Severe Acute Pancreatitis Detected by Positron Emission Tomography in ICR Mice. J Surg Res 2010;162:193-202. [DOI: 10.1016/j.jss.2009.06.011] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2008] [Revised: 05/26/2009] [Accepted: 06/09/2009] [Indexed: 01/20/2023]

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression. J Transl Med 2010;90:654-64. [PMID: 20157294 DOI: 10.1038/labinvest.2010.44] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open

Dahlhoff M, Algül H, Siveke JT, Lesina M, Wanke R, Wartmann T, Halangk W, Schmid RM, Wolf E, Schneider MR. Betacellulin protects from pancreatitis by activating stress-activated protein kinase. Gastroenterology 2010;138:1585-94, 1594.e1-3. [PMID: 20038432 DOI: 10.1053/j.gastro.2009.12.045] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/12/2009] [Revised: 11/25/2009] [Accepted: 12/15/2009] [Indexed: 12/21/2022]

Mann O, Kaifi J, Bloechle C, Schneider CG, Yekebas E, Kluth D, Izbicki JR, Strate T. Therapeutic small-volume resuscitation preserves pancreatic microcirculation in acute experimental pancreatitis of graded severity in rats. Pancreatology 2009;9:652-61. [PMID: 19684429 DOI: 10.1159/000212100] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/04/2008] [Accepted: 08/21/2008] [Indexed: 12/11/2022]

Price-Forbes AN, Filer A, Udeshi UL, Rai A. Progression of imaging in pancreatitis panniculitis polyarthritis (PPP) syndrome. Scand J Rheumatol 2009;35:72-4. [PMID: 16467048 DOI: 10.1080/03009740500228073] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022]

Polyarthritis with chondronecrosis associated with osteonecrosis, panniculitis and pancreatitis. Rheumatol Int 2009;30:1239-42. [PMID: 19575201 DOI: 10.1007/s00296-009-1046-9] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/28/2009] [Accepted: 06/21/2009] [Indexed: 10/20/2022]

Ríos-Fernández R, Callejas-Rubio JL, Sánchez-Cano D, Martín-Ruiz JL, Ortego-Centeno N. [Paniculitis, polyarthritis and pancreatitis]. Rev Clin Esp 2008;208:156-7. [PMID: 18275770 DOI: 10.1157/13115824] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]

Redox status of acute pancreatitis as measured by cyclic voltammetry: initial rodent studies to assess disease severity. Crit Care Med 2008;36:866-72. [PMID: 18431274 DOI: 10.1097/ccm.0b013e318165fa7f] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]

Abstract

OBJECTIVE

To determine whether serum antioxidant capacity as measured by the electrochemical technique cyclic voltammetry could be used to resolve differences in the severity of an inflammatory disease such as acute pancreatitis.

DESIGN

Experimental animal study.

SETTING

Animal laboratory, Department of Surgery, Faculty of Medical and Health Sciences, University of Auckland, New Zealand.

SUBJECTS

Male Wistar rats.

INTERVENTIONS

A total of 48 inbred male Wistar rats were studied in five experimental groups. Group 1 (baseline reference, immediate euthanasia, n = 14) had no surgical intervention. Group 2 (sham, n = 9) had identical surgical procedures to the pancreatitis groups except for the intraductal infusion. Groups 3-5 (n = 9, n = 10, and n = 6, respectively) had acute pancreatitis induced by the pancreatic intraductal infusion of 3%, 4%, or 5% sodium taurocholate, respectively. Groups 2-5 were killed after 12 hrs.

MEASUREMENTS AND MAIN RESULTS

Cyclic voltammetry involves scanning the voltage of a working electrode while recording the anodic current produced as the low molecular weight antioxidants in the solution are oxidized on the surface of the working electrode. The current produced is proportional to the combined concentration of the antioxidants. There was a significant positive correlation of the first cyclic voltammetric peak maximum with pancreatic histologic severity (Spearman's r = .51, p = .007) and with a number of other markers of systemic severity, notably bicarbonate (r = -.57, p = .002), base excess (r = -.65, p < .001), urea (r = .68, p < .001), and calcium (r = -.60, p = .008). The first cyclic voltammetric peak maximum was superior at indicating the severity of the disease state compared with a standard method of total antioxidant capacity measurement.

CONCLUSIONS

In experimental pancreatitis, the first cyclic voltammetric peak maximum showed significant correlations with histologic and systemic indices of severity. Further clinical studies are now needed to define the role of cyclic voltammetry in monitoring the progression of this and other severe illness in the critical care setting.

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Characterisation of a transgenic mouse expressing R122H human cationic trypsinogen. BMC Gastroenterol 2006;6:30. [PMID: 17069643 PMCID: PMC1637108 DOI: 10.1186/1471-230x-6-30] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/15/2006] [Accepted: 10/27/2006] [Indexed: 11/10/2022] Open

Alsfasser G, Warshaw AL, Thayer SP, Antoniu B, Laposata M, Lewandrowski KB, Fernández-del Castillo C. Decreased inflammation and improved survival with recombinant human activated protein C treatment in experimental acute pancreatitis. ACTA ACUST UNITED AC 2006;141:670-6; discussion 676-7. [PMID: 16847238 PMCID: PMC3972126 DOI: 10.1001/archsurg.141.7.670] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]

Ponzo O, Schreier L, Resnik R, Negri G, Scacchi P, Cresta MA, Wikinski R. Endogenous hypertriglyceridemia intensifies the course of cerulein-induced pancreatitis in rat: relation with changes in the VLDL composition. ANNALS OF NUTRITION AND METABOLISM 2005;50:37-44. [PMID: 16276074 DOI: 10.1159/000089563] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Subscribe] [Scholar Register] [Received: 11/26/2004] [Accepted: 05/12/2005] [Indexed: 01/31/2023]

Ramos O, Leitão OR, Repka JCD, Barros SGDS. Pancreatite aguda experimental induzida pela L-arginina: avaliação histológica e bioquímica. ARQUIVOS DE GASTROENTEROLOGIA 2005;42:55-9. [PMID: 15976912 DOI: 10.1590/s0004-28032005000100012] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/03/2023]

Abstract RACIONAL: Doses excessivas de aminoácidos básicos como a L-arginina têm a capacidade de lesar o pâncreas de ratos. OBJETIVO: Descrever e avaliar as características bioquímicas e histológicas da pancreatite aguda induzida pela L-arginina em ratos durante a instalação, desenvolvimento e reparação do processo inflamatório pancreático. MATERIAL E MÉTODOS: A amostra constituiu-se de 105 ratos machos, da linhagem Wistar. Aos ratos do grupo experimento (n = 70) administrou-se injeção intraperitonial de 500 mg/100 g de peso corporal de L-arginina. No grupo controle (n = 35) foi injetada solução salina isotônica. Analisaram-se 10 animais do grupo experimento e 5 do grupo controle em cada período de 6 h, 12 h, 24 h, 48 h, 72 h, 7 dias e 14 dias. Durante os tempos determinados coletou-se sangue para exames laboratoriais e o pâncreas para análise em microscopia óptica. RESULTADOS: Doze a 24 horas após a injeção de L-arginina os níveis séricos de amilase atingiram valores máximos, comparados àqueles dos ratos controle, decrescendo gradualmente, alcançou-os na 48ªhora sendo significativamente menor após 72 horas e 7 dias. A atividade enzimática retornou a níveis basais após 14 dias. Os valores de amilase estavam normais em todos os tempos avaliados nos animais do grupo controle. Na microscopia óptica, após injeção de L-arginina, observou-se arquitetura pancreática histologicamente preservada no período de 6 horas, evidenciando-se em 24 horas importante edema intersticial. Após 48 horas, a arquitetura acinar estava parcialmente destruída com necrose celular focal, atingindo sua máxima severidade ao ultrapassar 72 horas. No 7º dia a necrose tecidual e o edema haviam diminuído, iniciando-se a regeneração da arquitetura acinar. Observou-se a reconstrução estrutural pancreática após 14 dias. No grupo controle não se encontraram alterações histológicas pancreáticas. CONCLUSÃO: A pancreatite aguda experimental induzida pela L-arginina induz a necrose pancreática, apresentando evolução auto-limitada com regeneração do pâncreas em 2 semanas. Collapse

Top PC, Tissing WJE, Kuiper JW, Pieters R, van Eijck CHJ. L-asparaginase-induced severe necrotizing pancreatitis successfully treated with percutaneous drainage. Pediatr Blood Cancer 2005;44:95-7. [PMID: 15368548 DOI: 10.1002/pbc.20187] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/19/2023]