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 H2O2 (0, 50, 100, 250, 500 micromol/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, H2O2, and quercetin + H2O2 groups. For the quercetin groups, the cells were treated with different concentrations of quercetin (0, 10, 25, 50 micromol/L) before exposure to H2O2. 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 (DeltaPsim) changes were detected by flow cytometry. RESULTS: An oxidative stress model of HaCaT cells was established under a suitable concentration (250 micromol/L) and treated time of H2O2 (2 hours). The cell viability and DeltaPsim decreased in a concentration-dependent and time-dependent manner while the percentage of apoptotic cells significantly increased in the H2O2 groups compared with the control group (P < 0.05). The cell viability and DeltaPsim of the quercetin treated group increased (P < 0.05) and the percentage of apoptotic cells decreased at concentrations of 1-50 micromol/L quercetin (P < 0.01) compared with H2O2 treated group. CONCLUSION: Quercetin can relieve the cell damage and apoptosis from H2O2 induced injury to HaCaT cells by anti-oxidation and mitochondrial protection.
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 H2O2 (0, 50, 100, 250, 500 micromol/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, H2O2, and quercetin + H2O2 groups. For the quercetin groups, the cells were treated with different concentrations of quercetin (0, 10, 25, 50 micromol/L) before exposure to H2O2. 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 (DeltaPsim) changes were detected by flow cytometry. RESULTS: An oxidative stress model of HaCaT cells was established under a suitable concentration (250 micromol/L) and treated time of H2O2 (2 hours). The cell viability and DeltaPsim decreased in a concentration-dependent and time-dependent manner while the percentage of apoptotic cells significantly increased in the H2O2 groups compared with the control group (P < 0.05). The cell viability and DeltaPsim of the quercetin treated group increased (P < 0.05) and the percentage of apoptotic cells decreased at concentrations of 1-50 micromol/L quercetin (P < 0.01) compared with H2O2 treated group. CONCLUSION:Quercetin can relieve the cell damage and apoptosis from H2O2 induced injury to HaCaT cells by anti-oxidation and mitochondrial protection.