Baicalin alleviates the injury of human retinal pigment epithelium cells and improves branch retinal vein occlusion in rats by inhibiting the HIF-1α/VEGFA axis

Abstract Background At present, relevant studies have found that baicalin can improve macular edema (ME) caused by glaucoma, but the effect on branch retinal vein occlusion (BRVO) is still unclear. Methods The CoCl2-stimulated ARPE-19 cells were treated with different concentrations of baicalin and detected cell viability, apoptosis and oxidative stress. Next, the hypoxia-inducible factor-1α (HIF-1α) overexpression vector or siRNA were transfected into CoCl2-stimulated ARPE-19 cells, and the cell changes were detected. We searched the potential binding proteins of HIF-1α through the online database, and screened vascular endothelial growth factor A (VEGFA) as the research object. The CoCl2-stimulated ARPE-19 cells were treated with baicalin alone, or transfected with HIF-1α overexpression vector, or transfected with HIF-1α overexpression vector and VEGFA siRNA, and the cell changes were detected. Finally, we verified the therapeutic effect of baicalin on BRVO rats in vivo. Results Baicalin inhibited CoCl2-induced apoptosis, inflammation and oxidative stress in ARPE-19 cells, and baicalin inhibited HIF-1α protein expression. In CoCl2-induced hypoxia cells, HIF-1α aggravated apoptosis, inflammation and oxidative stress, while HIF-1α silencing alleviated cell damage. Mechanism study showed that in baicalin-treated CoCl2-induced cells, VEGFA protein expression decreased and cell damage was improved, but this protective effect was counteracted by HIF-1α, and VEGFA silencing again inhibited apoptosis, inflammation and oxidative stress. Baicalin inhibited HIF-1α and VEGFA protein expression in the retinal tissue of BRVO rats, reduced injury, and promoted the recovery of ganglion cell layer. Conclusions Baicalin alleviated ARPE-19 cell injury and improved BRVO in rats by inhibiting HIF-1α/VEGFA axis in vivo and in vitro.