Song MY, Bae UJ, Lee BH, Kwon KB, Seo EA, Park SJ, Kim MS, Song HJ, Kwon KS, Park JW, Ryu DG, Park BH. Nardostachys jatamansi extract protects against cytokine-induced β-cell damage and streptozotocin-induced diabetes. World J Gastroenterol 2010; 16(26): 3249-3257 [PMID: 20614480 DOI: 10.3748/wjg.v16.i26.3249]
Corresponding Author of This Article
Byung-Hyun Park, MD, PhD, Department of Biochemistry, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk 561-756, South Korea. bhpark@jbnu.ac.kr
Article-Type of This Article
Original Article
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jul 14, 2010; 16(26): 3249-3257 Published online Jul 14, 2010. doi: 10.3748/wjg.v16.i26.3249
Nardostachys jatamansi extract protects against cytokine-induced β-cell damage and streptozotocin-induced diabetes
Mi-Young Song, Ui-Jin Bae, Bong-Hee Lee, Kang-Beom Kwon, Eun-A Seo, Sung-Joo Park, Min-Sun Kim, Ho-Joon Song, Keun-Sang Kwon, Jin-Woo Park, Do-Gon Ryu, Byung-Hyun Park
Mi-Young Song, Jin-Woo Park, Byung-Hyun Park, Department of Biochemistry, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk 561-756, South Korea
Ui-Jin Bae, Bong-Hee Lee, Kang-Beom Kwon, Do-Gon Ryu, Department of Physiology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, South Korea
Eun-A Seo, Department of Food and Nutrition, School of Human Environmental Science, Wonkwang University, Iksan, Jeonbuk 570-749, South Korea
Sung-Joo Park, Min-Sun Kim, Ho-Joon Song, Department of Herbology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, South Korea
Keun-Sang Kwon, Department of Preventive Medicine, Medical School, Chonbuk National University, Jeonju, Jeonbuk 561-756, South Korea
Author contributions: Song MY and Bae UJ contributed equally to this work; Song MY and Bae UJ performed the research; Kwon KB, Seo EA and Park JW designed the research; Park SJ, Kim MS and Song HJ prepared Nardostachys jatamansi extract; Lee BH performed the research; Kwon KS analyzed the data; Ryu DG and Park BH wrote the paper.
Supported by Grant from the Ministry of Science and Technology/Korea Science and Engineering Foundation through the Diabetes Research Center at Chonbuk National University, R13-2008-005-0000-0, and by a Research Fund of Chonbuk National University in 2009 (to Park BH)
Correspondence to: Byung-Hyun Park, MD, PhD, Department of Biochemistry, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk 561-756, South Korea. bhpark@jbnu.ac.kr
Telephone: +82-63-2703139 Fax: +82-63-2749833
Received: February 3, 2010 Revised: March 17, 2010 Accepted: March 24, 2010 Published online: July 14, 2010
Abstract
AIM: To investigate the anti-diabetogenic mechanism of Nardostachys jatamansi extract (NJE).
METHODS: Mice were injected with streptozotocin via a tail vein to induce diabetes. Rat insulinoma RINm5F cells and isolated rat islets were treated with interleukin-1β and interferon-γ to induce cytotoxicity.
RESULTS: Treatment of mice with streptozotocin resulted in hyperglycemia and hypoinsulinemia, which was confirmed by immunohistochemical staining of the islets. The diabetogenic effects of streptozotocin were completely abolished when mice were pretreated with NJE. Inhibition of streptozotocin-induced hyperglycemia by NJE was mediated by suppression of nuclear factor (NF)-κB activation. In addition, NJE protected against cytokine-mediated cytotoxicity. Incubation of RINm5F cells and islets with NJE resulted in a significant reduction in cytokine-induced NF-κB activation and downstream events, inducible nitric oxide synthase expression and nitric oxide production. The protective effect of NJE was further demonstrated by the normal insulin secretion of cytokine-treated islets in response to glucose.
CONCLUSION: NJE provided resistance to pancreatic β-cell damage from cytokine or streptozotocin treatment. The β-cell protective effect of NJE is mediated by suppressing NF-κB activation.
