METHODS:In vitro cultured RF/6A cells were randomly divided into the control group, hypoxic injury(induced by CoCl2 stimulation)group and hypoxic injury + adiponectin(5μmol/L, 50μmol/L and 100μmol/L)group. Cell viability was assessed using the MTT assay and optimal concentration of adiponectin was selected. Western blot was used to detect the expression of Bax and Bcl-2 in RF/6A cells. Reactive oxygen species(ROS)detection kit was used to detect the content of ROS in RF/6A cells.

RESULTS: Compared with the control group, the cell viability of RF/6A cells in the hypoxic injury group and each adiponectin pretreatment group decreased(all P<0.01). Compared with the hypoxic injury group, the cell viability of RF/6A cells in each adiponectin pretreatment group was significantly increased(all P<0.05), and adiponectin of 50μmol/L was the appropriate protective concentration. Compared with the control group, the viability of RF/6A cells decreased, the protein expression level of Bax increased, the protein expression level of Bcl-2 decreased, and the content of ROS increased in the hypoxic injury group(all P<0.01). Compared with the hypoxic injury group, the viability RF/6A cells increased, the expression level of Bax decreased, the expression level of Bcl-2 increased, and the content of ROS decreased in the adiponectin pretreatment group(all P<0.01).

CONCLUSION: Our findings suggest that adiponectin can significantly alleviate retinal vascular endothelial cell damage and apoptosis caused by hypoxia, and the mechanism may be related to the inhibition of oxidative stress by adiponectin.