Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Effect of ursolic acid on obesity-induced insulin resistance in rat liver

Wang Ziwei¹, Zhou Na¹, Fang Shengbo², Zhang Xin²

¹Department of Pharmacy, School and Hospital of Stomatology, Jilin University; ²Department of Pharmacy, First Hospital of Jilin University, Changchun City, China.

For correspondence:- Zhang Xin Email: ms0746@163.com Tel:+8643185579358

Accepted: 22 April 2018 Published: 28 May 2018

Citation: Ziwei W, Na Z, Shengbo F, Xin Z. Effect of ursolic acid on obesity-induced insulin resistance in rat liver. Trop J Pharm Res 2018; 17(5):837-842 doi: 10.4314/tjpr.v17i5.13

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the expression of protein tyrosine phosphatase-1B (PTP-1B) and insulin receptor substrate-2 (IRS-2) in the liver tissue of obesity-induced insulin-resistant rats.

Methods: Insulin resistance (IR) was induced in Wistar rats by placing them on a high fat diet for 6 weeks, and ursolic acid (UA) was administered. Metformin served as positive control drug. The rats were divided into 5 groups based on the treatments given: normal group, positive control group, metformin group, high-dose UA group, and low-dose UA group. The general conditions of the rats were assessed 4 and 8 weeks after the various treatments. Liver glycogen levels were measured, and liver histological examination carried out after tissue processing and staining with hematoxylin and eosin (H & E). Real-time polymerase chain reaction (RT-PCR) was employed for the determination of hepatic expressions of PTP-1B and IRS-2 mRNAs, while expressions of PTP-1B protein and IRS-2 protein, and phosphorylation of IRS-2 tyrosine were assayed by Western blotting.

Results: Liver glycogen levels were significantly increased in the UA-treated groups (p < 0.05). Moreover, UA provoked reductions in the expression of PTP-1B protein (p < 0.05), but up-regulated the expression of IRS-2 protein (p < 0.05), and enhanced IRS-2 tyrosine phosphorylation (p < 0.05).

Conclusion: These results suggest that UA mitigates IR through blockage of PTP-1B expression and up-regulation of the expression of IRS-2 mRNA. Therefore, PTP-1B is a potential target for the treatment of type 2 diabetes.

Keywords: Ursolic acid, Insulin resistance, Liver, Protein tyrosine phosphatase-1B, Insulin receptor substrate-2