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Quercetin Mitigates Hepatic Insulin Resistance in Rats with Bile Duct Ligation Through Modulation of the STAT3/SOCS3/IRS1 Signaling Pathway
Author(s) -
Khodarahmi Ameneh,
Eshaghian Azam,
Safari Fatemeh,
Moradi Ali
Publication year - 2019
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.14793
Subject(s) - insulin resistance , hepatic fibrosis , quercetin , medicine , endocrinology , fibrosis , downregulation and upregulation , western blot , chemistry , pharmacology , insulin , biochemistry , antioxidant , gene
Insulin resistance (IR) and inflammatory mediators are correlated with hepatic fibrosis. Quercetin is a bioflavonoid with well‐known antidiabetic and antifibrotic properties. Bile duct ligation (BDL) is a surgical model performed on animals to produce a murine model in which increased oxidative stress occurs, which results in liver fibrosis. Our study aimed to determine whether quercetin improves hepatic IR as well as hepatic fibrosis in rats experiencing BDL. Male Wistar rats were allocated to four groups according to a random pattern, including a sham group, a sham and quercetin group (30 mg/kg/day), a BDL alone group, and a BDL and quercetin group (30 mg/kg/day). Evaluation of STAT3, SOCS3, IRS1, Rac1, Rac1‐GTP, Sp1, NOX1, HIF‐1α, and ERK1 expression was performed by RT‐PCR along with the western blot analytical technique in liver tissue. The antidiabetic impact of quercetin was associated with reduction in mRNA and expression of protein in STAT3 and SOCS3, along with an increase in IRS1. The antifibrotic effect of quercetin was also determined by downregulation of mRNA or the levels of protein expression of Rac1‐GTP, Rac1, HIF‐1α, NOX1, and Sp1, along with ERK1. Our study indicates that quercetin may improve hepatic fibrosis via inhibiting ROS‐associated inflammation as well as ameliorating hepatic IR by beneficial regulation of the STAT3/SOCS3/IRS1 signaling pathway.