Lou Y, Luan YT, Rong WQ, Gai Y. Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagy via the SIRT1-AMPK pathway. World J Diabetes 2024; 15(9): 1916-1931 [PMID: 39280180 DOI: 10.4239/wjd.v15.i9.1916]
Corresponding Author of This Article
Yun Gai, PhD, Chief Physician, Department of General Practice (Including Medical Oncology), Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, No. 358 Datong Road, Shanghai 200137, China. gaiyunlucky@163.com
Research Domain of This Article
Urology & Nephrology
Article-Type of This Article
Basic Study
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Lou Y, Luan YT, Rong WQ, Gai Y. Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagy via the SIRT1-AMPK pathway. World J Diabetes 2024; 15(9): 1916-1931 [PMID: 39280180 DOI: 10.4239/wjd.v15.i9.1916]
World J Diabetes. Sep 15, 2024; 15(9): 1916-1931 Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1916
Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagy via the SIRT1-AMPK pathway
Yu Lou, Yu-Ting Luan, Wen-Qing Rong, Yun Gai
Yu Lou, Department of Preventive Treatment of Disease, Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China
Yu-Ting Luan, Department of Infectious Diseases, Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China
Wen-Qing Rong, Yun Gai, Department of General Practice (Including Medical Oncology), Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China
Author contributions: Lou Y and Luan YT performed conceptualization, methodology, data curation, visualization, investigation, and writing of the original draft; Rong WQ was responsible for project administration; Gai Y was responsible for supervision, funding acquisition, resources, and review and editing of the manuscript. Lou Y and Luan YT contributed equally to this work.
Supported byShanghai Pudong New Area Leading Talents Training Program Project, No. PWR12020-02; Shanghai Pudong New Area Excellent Young Medical Talents Training Program Project, No. PWRq2023-40; and Shanghai Pudong New Area Health and Family Planning Scientific Research Project, No. PW2022A-91.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Shanghai Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine.
Institutional animal care and use committee statement: The Animal Care and Use Committee of Shanghai Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine approved this entire study.
Conflict-of-interest statement: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Data sharing statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Corresponding author: Yun Gai, PhD, Chief Physician, Department of General Practice (Including Medical Oncology), Seventh People's Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, No. 358 Datong Road, Shanghai 200137, China. gaiyunlucky@163.com
Received: March 6, 2024 Revised: June 4, 2024 Accepted: July 2, 2024 Published online: September 15, 2024 Processing time: 174 Days and 4 Hours
Abstract
BACKGROUND
Diabetic nephropathy (DN) is the most frequent chronic microvascular consequence of diabetes, and podocyte injury and malfunction are closely related to the development of DN. Studies have shown that corilagin (Cor) has hepatoprotective, anti-inflammatory, antibacterial, antioxidant, anti-hypertensive, anti-diabetic, and anti-tumor activities.
AIM
To explore the protective effect of Cor against podocyte injury in DN mice and the underlying mechanisms.
METHODS
Streptozotocin and a high-fat diet were combined to generate DN mice models, which were then divided into either a Cor group or a DN group (n = 8 in each group). Mice in the Cor group were intraperitoneally injected with Cor (30 mg/kg/d) for 12 wk, and mice in the DN group were treated with saline. Biochemical analysis was used to measure the blood lipid profiles. Hematoxylin and eosin staining was used to detect pathological changes in kidney tissue. Immunohistochemistry and Western blotting were used to assess the protein expression of nephrin and podocin. Mouse podocyte cells (MPC5) were cultured and treated with glucose (5 mmol/L), Cor (50 μM), high glucose (HG) (30 mmol/L), and HG (30 mmol/L) plus Cor (50 μM). Real-time quantitative PCR and Western blotting were performed to examine the effects of Cor on podocyte autophagy.
RESULTS
Compared with the control group, the DN mice models had increased fasting blood glucose, glycosylated hemoglobin, triglycerides, and total cholesterol, decreased nephrin and podocin expression, increased apoptosis rate, elevated inflammatory cytokines, and enhanced oxidative stress. All of the conditions mentioned above were alleviated after intervention with Cor. In addition, Cor therapy improved SIRT1 and AMPK expression (P < 0.001), inhibited reactive oxygen species and oxidative stress, and elevated autophagy in HG-induced podocytes (P < 0.01).
CONCLUSION
Cor alleviates podocyte injury by regulating autophagy via the SIRT1-AMPK pathway, thereby exerting its protective impact on renal function in DN mice.
Core Tip: This study explored the protective effects of Corilagin (Cor) against podocyte injury in diabetic nephropathy (DN). Cor treatment markedly attenuated fasting blood glucose, glycosylated hemoglobin, triglycerides, and total cholesterol, increased nephrin and podocin expression, reduced apoptosis rate, and inhibited inflammatory cytokines and oxidative stress. In addition, Cor contributed to improving SIRT1 and AMPK expression, inhibited reactive oxygen species and oxidative stress, and elevated autophagy in high-glucose-treated podocytes. Thus, Cor might be a potential therapeutic agent for the treatment and clinical management of DN.
