Celastrol inhibits the proliferation and angiogenesis of high glucose-induced human retinal endothelial cells

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes. Celastrol plays a certain role in the improvement of various diabetes complications. Therefore, this study aimed to explore whether celastrol inhibited the proliferation and angiogenesis of high glucose (HG)-induced human retinal endothelial cells (hRECs) by down-regulating the HIF1/VEGF signaling pathway. The viability and proliferation of hRECs treated with glucose, celastrol or dimethyloxallyl glycine (DMOG) were analyzed by MTT assay. The invasion and tube formation ability of hRECs treated with glucose, celastrol or DMOG were in turn detected by transwell assay and tube formation assay. The expression of HIF1[alpha] and VEGF in hRECs after indicated treatment was analyzed by Western blot analysis and RT-qPCR analysis and ICAM-1 expression in hRECs after indicated treatment was detected by immunofluorescence assay HG induction promoted the proliferation, invasion and tube formation ability and increased the expression of HIF-1[alpha] and VEGF of hRECs, which were gradually suppressed by celastrol changing from 0.5 to 2.0 [mu]M. DMOG was regarded as a HIF1[alpha] agonist, which attenuated the effect of celastrol on HG-induced hRECs. Celastrol inhibited the proliferation and angiogenesis of HG-induced hRECs by down-regulating the HIF1[alpha]/VEGF signaling pathway.