Urantide protects CCl4-induced liver injury via inhibiting GPR14 signal in mice. Issue 1 (2nd January 2017)

• Record Type: Journal Article
• Authors: Sun, Haiying; Zhang, Lin; Shen, Dan
• Is Part Of: Biotechnology, biotechnological equipment. Volume 31:Issue 1(2017)
• Page Start: 156
• Page End: 161
• Publication Date: 2017-01-02
• Subjects: UII/GPR14 -- inflammation -- oxidative stress; Biotechnology -- Periodicals; Biotechnology -- Periodicals; Biotechnology -- instrumentation -- Periodicals; Periodicals; 660.605
• DOI: 10.1080/13102818.2016.1253436
• Languages: English
• ISSNs: 1310-2818

Abstract

ABSTRACT: Previous reports suggest that rotensin II (UII) and its G protein-coupled receptor (GPR14) involve in inflammatory mediation, while the effects of UII/GPR14 in liver inflammatory response are not fully illustrated. Thus, in this study, urantide, a special antagonist of GPR14, was used to investigate the effects of UII/GPR14 on carbon tetrachloride (CCl4 ) induced liver injury in mice. The results showed that CCl4 upregulated liver UII and GPR14 expression. Meanwhile, CCl4 caused liver injury, inflammation and oxidative stress. Injection of urantide alleviated CCl4 -induced inflammatory response and oxidative stress, which might further exhibit a hepatoprotective effect. In conclusion, UII/GPR14 may serve as a potential target for therapeutic intervention in liver injury.