A reactive oxygen species activation mechanism contributes to Sophoridine-induced apoptosis in rat liver BRL-3A cells

Abstract

Ethnopharmacological relevanceSophora alopecuroides L., a traditional Chinese herb, has been widely used to treat numerous diseases throughout China. Quinolizidine alkaloids were identified as active components in Sophora alopecuroides L., and Sophoridine (SRI) is the major component in the Quinolizidine alkaloids. Aim of the studyTo investigate the toxic effects of SRI in rat liver BRL-3A cells and to explore potential ROS-related mechanisms. Materials and methodsCell viability, cytotoxicity, apoptosis, intracellular generation of ROS, GSH/GSSG ratio and levels of proteins in mitochondria apoptosis pathway were analyzed. ResultsOur data indicated that SRI could suppress BRL-3A cells viability in a concentration- and time-dependent manner and increase cytotoxicity, ROS accumulation and cell apoptosis in a concentration-dependent manner. Expressions and activities of apoptotic related proteins were upregulated, whereas expression of Bcl-2 was downregulated after treatment. Furthermore, level of H2O2 was increased, whereas level of Superoxide was not changed after treatment. Moreover, the antioxidant N-acetylcysteine reversed SRI-induced apoptosis and ROS accumulation. ConclusionOur data suggest that SRI promotes rat liver BRL-3A cells apoptosis by increasing intracellular ROS accumulation.