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Mol Cell Biochem. 2019 Jun 10. doi: 10.1007/s11010-019-03572-1. [Epub ahead of print]

Attenuating effect of silibinin on palmitic acid-induced apoptosis and mitochondrial dysfunction in pancreatic β-cells is mediated by estrogen receptor alpha.

Author information

1
Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, People's Republic of China.
2
Department of Pharmacy, The Third People's Hospital of Chengdu, Chengdu, 610031, Sichuan, People's Republic of China.
3
School of Traditional Chinese Medica, Shenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China.
4
Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, People's Republic of China.
5
Department of Chemistry and Life Science, School of Advanced Engineering, Kogakuin University, 2665-1, Nakanomachi, Hachioji, Tokyo, 192-0015, Japan.
6
Department of Clinical and Pharmaceutical Sciences, Showa Pharmaceutical University, Tokyo, 194-8543, Japan.
7
Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, People's Republic of China. ikejimat@vip.sina.com.
8
Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, People's Republic of China. ikejimat@vip.sina.com.

Abstract

High levels of circulating free fatty acids often trigger pancreatic β cell dysfunction during the development of type 2 diabetes. Silibinin, the main component of Silybum marianum fruit extract (silymarin), is reported to have anti-diabetic effect. This study is designed to determine the protective effect of silibinin on palmitic acid-induced damage in a rat pancreatic β-cell line, INS-1 cells. Our results demonstrate that silibinin improves cell viability, enhances insulin synthesis and secretion, and resumes normal mitochondrial function in palmitic acid-treated INS-1 cells. An accumulating body of evidence has shown that the estrogen receptors are key molecules involved in glucose and lipid metabolism. Our results suggest that silibinin upregulates ERα signaling pathway from the finding that ERα-specific inhibitors abolish the anti-lipotoxic effect of silibinin. In conclusion, these findings suggest that silibinin protects INS-1 cells against apoptosis and mitochondrial damage through upregulation of ERα pathway.

KEYWORDS:

Estrogen receptors (ERs); Mitochondria; Palmitic acid; Silibinin

PMID:
31183735
DOI:
10.1007/s11010-019-03572-1

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