Salidroside attenuates diabetic retinopathy by upregulating miR-142-3p to target TRAF6.

This study aimed to investigate the role and molecular mechanisms of salidroside (SAL) in retinal vascular dysfunction under diabetic conditions. Human retinal microvascular endothelial cells (HRMECs) were cultured in a 30 mM high glucose (HG) medium to mimic diabetic conditions. Cell proliferation, migration, and angiogenesis were assessed by CCK-8, Transwell, and Matrigel tube formation assay, respectively. Tight junction-associated proteins ZO-1, occludin, and claudin-5 were detected by Western blot. The targeting relationship between miR-142-3p and TRAF6 was verified by bioinformatics analysis and dual-luciferase reporter gene assay. Retinal tissues from a streptozotocin (STZ)-induced diabetic rat model were examined by hematoxylin and eosin (HE) staining. SAL inhibited HG-induced proliferation, migration, and angiogenesis of HRMECs and promoted the expression of ZO-1, occludin, and claudin-5. SAL upregulated miR-142-3p expression, and miR-142-3p targeted TRAF6 to negatively regulate its expression. The inhibitory effects of SAL on HRMECs were reduced by lowering miR-142-3p or raising TRAF6 levels. SAL ameliorated retinopathy in diabetic rats. SAL attenuates diabetic retinal vascular dysfunction by upregulating miR-142-3p and downregulating TRAF6.