Suppression of oxidative stress and improvement of liver functions in mice by ursolic acid via LKB1‐AMP‐activated protein kinase signaling

• DOI: 10.1111/jgh.12723
• Publication Date: 2014-08-28T12:34:33Z
• Authors: Yongbin Yang; Zhanxue Zhao; Yuanjun Liu; Xianjiang Kang; Haisong Zhang; Ming Meng
• Keywords: Ursolic acid

Hepatic cirrhosis is the final stage of liver dysfunction, characterized by diffuse fibrosis, which main response to injury. This study investigate effects ursolic acid (UA) on functions and fibrosis in bile duct ligation (BDL) mice determine underlying mechanisms.Cultured hepatocytes were treated with lipopolysaccharide (LPS) presence or absence UA. The reactive oxygen species (ROS) level, protein levels IκBα, iNOS Cox-2, NF-κB activation detected, respectively. C57/BL6 AMP-activated kinase (AMPK)α2(-/-) subjected BDL for 14 days. UA was administered gavage. markers function oxidative stress, histopathology analyzed after treatment.Treatment dose-dependently activates AMPK, abolished silence B1 (LKB1). LPS significantly increased ROS productions, apoptosis, activation, expressions Cox-2 cultured hepatocytes. All these blocked co-incubation Importantly, LKB1, iNOS/Cox-2 small interference RNA transfection reversed UA-induced cells. In an animal study, 14-day induced injury, accompanied stress liver. Treatment attenuated BDL-induced detrimental wild-type but not AMPKα2(-/-) mice.UA via LKB1-AMPK signaling offers protective injury mice, may be related inhibition stress.