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.

Keywords: DNA damage; antioxidant; apoptosis; p-Coumaric acid; potassium bromate.