“…As shown in Figure , the hepatoprotective mechanisms of CPs could be explained by their potential capacity to prevent ROS‐related liver oxidative injury via eliminating oxygen, superoxide anion, and hydroxyethyl radicals, avoiding further activation of nuclear factor‐kappa B (NF‐κB), stress‐activated protein kinase (SAPK), and P53, all of which are stimulating factors in the death receptor‐mediated extrinsic pathway (Guo, Sun, He, Yu, & Du, ; Li et al., ). Additionally, CPs have been identified to markedly scavenge free radicals via lowered CHO, MDA, NO, HYP, TGF‐β1, TG, and LDH activities to the normal levels in organisms while restoring the contents of SOD, GPx, and GSH, all of which are known to be potent indicators of liver cytotoxicity (Lv et al., ; Wu et al., ; Yu et al., ). Moreover, CPs could also inhibit hepatocyte apoptosis via reducing the levels of tumor necrosis factor‐α (TNF‐α), cytochrome C, Fas, FasL, and caspase‐3 as well as increasing the Bcl‐2/Bax ratio, the key cytokines, or enzymes in the hepatocyte apoptosis pathway (Ma et al., ).…”