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Nutrients 2015, 7(6), 4689-4704; doi:10.3390/nu7064689

Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis

1
Department of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
2
Department of Pharmacology, Wannan Medical College, Wuhu 241002, China
3
Department of Pharmacy, Wannan Medical College, Wuhu 241002, China
4
Department of General Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 21 April 2015 / Revised: 28 May 2015 / Accepted: 1 June 2015 / Published: 9 June 2015
(This article belongs to the Special Issue Natural Products for Human Health)
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Abstract

Advanced glycation end products (AGEs), the direct modulators of β-cells, have been shown to cause insulin-producing β-cell dysfunction and apoptosis through increase of intracellular reactive oxygen species (ROS) production. Sesamin has been demonstrated to possess antioxidative activity. This study was designed to investigate whether sesamin protects against AGEs-evoked β-cell damage via its antioxidant property. The effects of sesamin were examined in C57BL/6J mice and MIN6 cell line. In in vivo studies, mice were intraperitoneally injected with AGEs (120 mg/kg) and orally treated with sesamin (160 mg/kg) for four weeks. Intraperitoneal glucose tolerance and insulin releasing tests were performed. Insulin content, ROS generation and β-cell apoptosis in pancreatic islets were also measured. In in vitro studies, MIN6 cells were pretreated with sesamin (50 or 100 μM) and then exposed to AGEs (200 mg/L) for 24 h. Insulin secretion, β-cell death, ROS production as well as expression and activity of NADPH oxidase were determined. Sesamin treatment obviously ameliorated AGE-induced β-cell dysfunction and apoptosis both in vivo and in vitro. These effects were associated with decreased ROS production, down-regulated expression of p67phox and p22phox, and reduced NADPH oxidase activity. These results suggest that sesamin protects β-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress. View Full-Text
Keywords: sesamin; advanced glycation end products; MIN6 cell; reactive oxygen species; apoptosis sesamin; advanced glycation end products; MIN6 cell; reactive oxygen species; apoptosis
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Kong, X.; Wang, G.-D.; Ma, M.-Z.; Deng, R.-Y.; Guo, L.-Q.; Zhang, J.-X.; Yang, J.-R.; Su, Q. Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis. Nutrients 2015, 7, 4689-4704.

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