l-carnitine attenuates oxidant injury in HK-2 cells via ROS-mitochondria pathway

Oxidative stress has been considered as the possible mechanism of renal ischemia/reperfusion injury. l-carnitine is an endogenous mitochondrial membrane compound and could effectively protect ischemia-reperfusion injury in the kidney. To elucidate the nephroprotective effects of l-carnitine, here we assessed the effect of l-carnitine on hydrogen peroxide (H2O2)-mediated oxidative stress in the human proximal tubule epithelial cell line, HK-2 cells. The results showed that pretreatment with l-carnitine 12 h inhibited H2O2-induced cell viability loss, intracellular reactive oxygen species generation and lipid peroxidation in a concentration-dependent manner. Also l-carnitine promoted endogenous antioxidant defense components including total antioxidative capacity, glutathione peroxidase, catalase and superoxide dismutase. In parallel, cell apoptosis triggered by H2O2 characterized with the DNA fragment and caspase-3 activity were also inhibited by l-carnitine. Furthermore, mitochondrial dysfunction associated with cell apoptosis including membrane potential loss, down-regulation of Bcl-2 and up-regulation of Bax and the release of cytochrome c were abrogated in the presence of l-carnitine. These results suggested that l-carnitine could protect HK-2 cells from H2O2-induced injury through the inhibition of oxidative damage, mitochondria dysfunction and ultimately inhibition of cell apoptosis, which indicates that l-carnitine may be a promising approach for the treatment of oxidative stress in renal diseases.