作者
Li Li,Qinghai Liu,Long Fan,Wei Xiao,Lei Zhao,Yu Wang,Weiguang Ye,Fei Lan,Bin Jia,Hua Feng,Changman Zhou,Xiuqin Yue,Guo‐Gang Xing,Tianlong Wang
摘要
// Li Li 1 , Qinghai Liu 1 , Long Fan 1 , Wei Xiao 1 , Lei Zhao 1 , Yu Wang 1 , Weiguang Ye 1 , Fei Lan 1 , Bin Jia 1 , Hua Feng 1 , Changman Zhou 2 , Xiuqin Yue 3 , Guogang Xing 4 , Tianlong Wang 1 1 Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing, China 2 Department of Anatomy & Histology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China 3 Department of Anesthesiology, the First Affiliated Hospital of Xinxiang Medical University, Henan, China 4 Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China Correspondence to: Guogang Xing, email: li_limzk@163.com Tianlong Wang, email: w_tl5595@hotmail.com Keywords: oxymatrine, arsenic trioxide, liver, HO-1, Nrf-2 Received: July 25, 2016 Accepted: September 06, 2016 Published: October 5, 2016 ABSTRACT Oxymatrine, a quinolizidine natural drug extracted from Sophora japonica , has been reported to have neuroprotective effect and cardioprotective effect. However, the protective effect of oxymatrine on arsenic trioxide (As 2 O 3 )-induced liver injury has not been reported. In the present study, we investigated the protective effects of oxymatrine on As 2 O 3 -induced liver injury in rats. Male Wistar rats were administrated 3mg/kg As 2 O 3 intravenous injection on alternate days for 4 days. Oxymatrine was given 1 h before As 2 O 3 treatment. The results showed that oxymatrine inhibited As 2 O 3 -induced hepatic pathological damage, liver ROS level and MDA level in a dose-dependent manner. As 2 O 3 decreased the antioxidant enzymes SOD, GPX, and CAT activity and the decrease was inhibited by treatment of oxymatrine. Furthermore, oxymatrine attenuated the retention of arsenic in liver tissues and improved the expression of Nrf2 and HO-1. In conclusion, our results suggested that oxymatrine protected against As 2 O 3 -induced oxidative damage by activating Nrf2/HO-1 signaling pathway.