MiR-19a inhibitor improves diabetic retinopathy in rats through PTEN/Akt/P-Akt signaling pathway

Abstract

The aim of this study is to explore the regulatory effect of micro ribonucleic acid (miR)-19a on diabetic retinopathy (DR) through mediating the phosphatase and tensin homolog deleted on chromosome ten (PTEN)/protein kinase B (Akt) signaling pathway. Thirty male Sprague-Dawley rats were first divided into Healthy group, DR group and miR-19a inhibitor group. The DR model was induced by intraperitoneal injection of streptozotocin (STZ) (60 mg/kg). The retinal tissues were dissected and RGCs were isolated. The expression level of miR-19a therein was determined using quantitative polymerase chain reaction (qPCR). The pathological changes were observed through hematoxylin-eosin staining (HE) staining. The apoptosis was detected by flow cytometry. PTEN was predicted as a target gene of miR-19a through TargetScan biological software. The protein expression of PTEN was detected via immunofluorescence assay. The changes in the phosphatidylinositol 3-hydroxy kinase (PI3K)/Akt pathway-associated proteins were detected using Western blotting. The expression of miR-19a declined substantially in DR rats injected with miR-19a inhibitor (P<0.05). RGCs were arranged regularly, showing apoptosis and milder necrosis in miR-19a inhibitor group. The proportion of apoptotic cells was substantially decreased in miR-19a inhibitor group (P<0.05). It was found that miR-19a inhibitor group exhibited an evidently lower protein expression of PTEN and a higher activation degree of the Akt pathway than DR group (P<0.05). MiR-19a binds to PTEN protein in a targeted manner to mediate the PI3K/Akt pathway, thereby affecting the progression of DR.