Quercetin in combating H2O2 induced early cell apoptosis and mitochondrial damage to normal human keratinocytes.

Background Oxidative stress plays an important role in the pathogenesis of epidermal diseases. This study aimed to investigate the effects of quercetin on the anti-oxidative response and on mitochondrial protection in cultured normal human keratinocytes. Methods Cultured HaCaT cells were treated with different concentrations of H 2 O 2 (0, 50, 100, 250, 500 μmol/L) for different periods of time (0.5, 1, 2, 4 hours) to establish an oxidative stress model. The cultured HaCaT cells were randomly assigned to control, H 2 O 2 , and quercetin+H 2 0 2 groups. For the quercetin groups, the cells were treated with different concentrations of quercetin (0, 10, 25, 50 μmol/L) before exposure to H 2 O 2 . Morphological changes of the cells were observed under an inverted microscope and an electron microscope. The cell viability was detected by the MTT method. The cell apoptosis (AnnexinV/propidium iodide double stain) and mitochondrial membrane potential (ΔΨm) changes were detected by flow cytometry. Results An oxidative stress model of HaCaT cells was established under a suitable concentration (250 μmol/L) and treated time of H 2 O 2 (2 hours). The cell viability and ΔΨm decreased in a concentration-dependent and time-dependent manner while the percentage of apoptotic cells significantly increased in the H 2 O 2 groups compared with the control group (P <0.05). The cell viability and ΔΨm of the quercetin treated group increased (P <0.05) and the percentage of apoptotic cells decreased at concentrations of 1―50 μmol/L quercetin (P <0.01 ) compared with H 2 O 2 treated group. Conclusion Quercetin can relieve the cell damage and apoptosis from H 2 O 2 induced injury to HaCaT cells by anti-oxidation and mitochondrial protection.