No protective effect of curcumin on hydrogen peroxide-induced cytotoxicity in HepG2 cells

Scavenging of intracellular reactive oxygen species (ROS) is one of the potential mechanisms contributing to the protective effects of many antioxidants. Curcumin, a natural product, is an effective ROS scavenger. However, the role of its ROS scavenging ability in its cytoprotective action remains to be clarified. Herein, the protective effects of curcumin on hydrogen peroxide (H2O2)- and tert-butyl hydroperoxide-induced ROS formation and HepG2 cell injury were determined. HepG2 cells were pretreated with curcumin for 30 min and then treated with H2O2 (500 mu M) or tert-butyl hydroperoxide (200 mu M) for 24 h. Curcumin pretreatment dramatically decreased H2O2- and tert-butyl hydroperoxide-induced ROS production, but failed to suppress cytotoxicity of those compounds. H2O2 induced decreases in mitochondrial membrane potential (Delta psi m) and increases in DNA fragmentation could not be reversed by curcumin. Furthermore, curcumin enhanced expression of H2O2-induced pro-apoptotic protein Bax expression and inhibited expression of anti-apoptotic proteins Bcl-2 and Bcl-xL. In addition, curcumin significantly decreased p38MAPK and phospho-CDC-2 protein expression and increased phospho-p38MAPK, p42/44MAPK, and phospho-p42/44MAPK protein expression. These results suggest that short pretreatment and subsequent longer co-treatment of low concentrations of curcumin showed no obvious protective effect on H2O2-induced HepG2 cell injury.