| Apoptosis of human corneal endothelial cells (HCECs) caused by reactive oxygen specie (ROS) has been implicated to be involved in several kinds of human keratopathy in recent years. Up to now, the inducing effect of ROS on HCECs apoptosis has been investigated mainly by clinical procedures which cost a lot of time and financing. And the broadness and advances of this kind of researches have been greatly limited. To provide the foundation for the clinic therapy of keratopathy caused by HCEC apoptosis, the effects of hydrogen peroxide (H2O2) and flavone on the apoptosis of HCECs, and the molecular antioxidant mechanisms of flavone were investigated with an HCEC cell line by light microscopy, AO/EB double-fluorescent staining, DNA electrophoresis and enzyme-linked immunosorbnent assay (ELISA) in this study.After treated with 200–800μmol/L of H2O2 respectively, cultured HCECs underwent apoptosis to different extents both in morphology, double-fluorescent staining and DNA electrophoresis, and the apoptotic extent was in a dose- and time-dependent manner. The HCECs underwent much remarkable apoptosis when treated with 800μmol/L H2O2 for 10h, and an obvious DNA ladder was found in electrophoresis.Treatment of 55 or 70μmol/L flavone did not cause any apoptosis of HCECs, while treatment of 85 and 100μmol/L flavone caused apoptosis of HCECs in a dose- and time- dependent manner. After treated with 85μmol/L flavone for 8h, HCECs underwent very remarkable apoptosis including apparent DNA fragmentation.After the HCECs pretreated with 55 or 70μmol/L flavone, HCEC apoptosis induced by 600μmol/L H2O2 had been greatly inhibited. In contrast, pretreatment of 85 or 100μmol/L flavone could not inhibit the H2O2-induced apoptosis of HCECs. The apoptosis-inhibiting effect of 70μmol/L flavone on HCECs was perfect enough and no DNA fragmentation was found at all. Therefore, it can be concluded that... |
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