Hepatoprotective effect of p‐Coumaric acid against KBrO₃‐induced apoptosis in HepG2 cells

Abstract

In the present study, we investigated the effect of the p‐Coumaric acid (PCA), a phenolic acid, on potassium bromate (KBrO₃) induced oxidative damage, Ras/Raf/MEK signaling, and apoptosis in HepG2 cells. Our findings showed that PCA‐treated cells prevented cytotoxicity compared with KBrO_3‐treated cells. Furthermore, KBrO₃‐induced oxidative stress and lipid peroxidation was attenuated by PCA and it also increased the antioxidant levels such as SOD, CAT, and GPX. Additionally, PCA inhibited the KBrO₃‐induced DNA damage in HepG2 cells. Moreover, PCA treatment suppressed the activation of Ras/Raf/MEK signaling and increased the expression of PRDX‐1. In addition, PCA prevented the KBrO₃‐induced apoptosis cascade by altering the expression of proapoptotic, Bax, caspase‐3, and antiapoptotic, Bcl‐2 proteins. The present study proves that PCA inhibited the KBrO₃‐induced oxidative stress, DNA damage, and apoptotic signaling cascade in HepG2 cells.