OBJECTIVE: To investigate the effects of resveratrol on the proliferation, apoptosis, mitochondrial membrane potential and cell morphology of human liver cancer cell line HepG2. METHODS: The changes in HepG2 cell growth and proliferation in response to resveratrol treatment were evaluated by MTT assay, and resveratrol-induced apoptosis of HepG2 cells was investigated by flow cytometry. Inverted microscope and electron microscope were employed for observing morphological changes of the treated cells. The whole-cell mitochondrial membrane potential was measured in separate experiments using two fluorimetric probes, rhodamine123 and TMRE, respectively. HepG2 cells treated with rhodamine123 were analyzed by flow cytometry and cells treated with TMRE by confocal microscope. RESULTS: MTT assay showed that low concentrations of resveratrol produced no significant effect on the growth of HepG2 cells, whereas at high concentrations, resveratrol could obviously inhibit the cell growth in a time- and dose-dependent manner. Resveratrol also induced apoptosis of HepG2 cells, and after a 24-hour treatment, resveratrol caused sharp increment of the mitochondria membrane potential. CONCLUSION: Resveratrol is capable of inhibiting the proliferation of HepG2 cells and inducing cell apoptosis by depolarizing mitochondrial membrane potential.
OBJECTIVE: To investigate the effects of resveratrol on the proliferation, apoptosis, mitochondrial membrane potential and cell morphology of humanliver cancer cell line HepG2. METHODS: The changes in HepG2 cell growth and proliferation in response to resveratrol treatment were evaluated by MTT assay, and resveratrol-induced apoptosis of HepG2 cells was investigated by flow cytometry. Inverted microscope and electron microscope were employed for observing morphological changes of the treated cells. The whole-cell mitochondrial membrane potential was measured in separate experiments using two fluorimetric probes, rhodamine123 and TMRE, respectively. HepG2 cells treated with rhodamine123 were analyzed by flow cytometry and cells treated with TMRE by confocal microscope. RESULTS:MTT assay showed that low concentrations of resveratrol produced no significant effect on the growth of HepG2 cells, whereas at high concentrations, resveratrol could obviously inhibit the cell growth in a time- and dose-dependent manner. Resveratrol also induced apoptosis of HepG2 cells, and after a 24-hour treatment, resveratrol caused sharp increment of the mitochondria membrane potential. CONCLUSION:Resveratrol is capable of inhibiting the proliferation of HepG2 cells and inducing cell apoptosis by depolarizing mitochondrial membrane potential.