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

Abstract

AbstractIn 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 KBrO3‐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.