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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 9651371, 6 pages
https://doi.org/10.1155/2017/9651371
Research Article

Salidroside Modulates Insulin Signaling in a Rat Model of Nonalcoholic Steatohepatitis

1Department of Hepatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, China
2Medical School of Ningbo University, Ningbo, Zhejiang 315211, China

Correspondence should be addressed to Hongshan Li; moc.621@2891_nahsgnohil

Received 17 November 2016; Revised 10 January 2017; Accepted 11 January 2017; Published 1 February 2017

Academic Editor: Jae Youl Cho

Copyright © 2017 Hongshan Li et al. 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.

Abstract

A growing body of evidence has shown the beneficial effects of salidroside in cardiovascular and metabolic diseases. This study aimed to evaluate the therapeutic effects of salidroside on nonalcoholic steatohepatitis (NASH) in rats and explore the underlying mechanisms related to insulin signaling. A rat model of NASH was developed by high-fat diet for 14 weeks. From week 9 onward, the treatment group received oral salidroside (4.33 mg/kg) daily for 6 weeks. Salidroside effectively attenuated steatosis and vacuolation of hepatic tissue, with a dramatic decrease in liver triglycerides and free fatty acid levels (P < 0.01). Dysregulation of FINS, FBG, HOMA-IR, ALT, and AST in serum was ameliorated with salidroside treatment (P < 0.01). In the liver, salidroside induced significant increases in key molecules in the insulin signaling pathway, such as phosphorylated insulin receptor substrate 1 (IRS1), phosphoinositide 3-kinase (PI3K), and protein kinase B (PKB), with a significant decrease in SREBP-1c levels (P < 0.01). Therefore, salidroside effectively protected rats from high-fat-diet-induced NASH, which may be partially attributed to its effects on the hepatic insulin signaling pathway.