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 CoCl(2)-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 CoCl(2)-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 CoCl(2)-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 CoCl(2)-induced apoptosis, inflammation and oxidative stress in ARPE-19 cells, and baicalin inhibited HIF-1α protein expression. In CoCl(2)-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 CoCl(2)-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.