MiR-182 inhibits oxidative stress and epithelial cell apoptosis in lens of cataract rats through PI3K/Akt signaling pathway

OBJECTIVE: The aim of this study was to investigate the influences of micro ribonucleic acid (miR)-182 on oxidative stress and epithelial cell apoptosis in the lens of cataract rats through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly assigned into three groups, including normal group (n=12), model group (n=12), and miR-182 mimics group (n=12). Rats in normal group were first normally fed. After establishing the cataract model, rats in model group were intraperitoneally injected with normal saline. Meanwhile, rats in miR-182 mimics group were intraperitoneally injected with miR-182 mimics. At 7 d after operation, materials were sampled. The expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were detected via immunofluorescence. The protein expressions of PI3K and Akt were detected using Western blotting. Moreover. the expression level of miR-182 was measured via qPCR. Cell apoptosis was evaluated using terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL). In addition, the content of superoxide dismutase (SOD) and malondialdehyde (MDA) was determined using enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared with normal group, both model group and miR-182 mimics group exhibited significantly up-regulated expression level of Bax and down-regulated expression of Bcl-2 (p<0.05). MiR-182 mimics group had markedly lower expression level of Bax and higher expression level of Bcl-2 than model group (p<0.05). Western blotting results demonstrated that the protein expression levels of PI3K and Akt in model and miR-182 mimics groups were considerably higher than those in normal group (p<0.05). Meanwhile. their protein expression levels in miR-182 mimics group were significantly higher than those in model group (p<0.05). In comparison with normal group, the expression level of miR-182 was markedly up-regulated in both model group and miR-182 mimics group (p<0.05). Moreover, its expression level in miR-182 mimics group was considerably higher than that in model group (p<0.05). TUNEL-positive cells increased significantly in both model group and miR-182 mimics group when compared with normal group (p<0.05). However, they were remarkably reduced in miR-182 mimics group when compared with model group (p<0.05). Compared with normal group, model and miR-182 groups exhibited substantially decreased SOD content and increased MDA content (p<0.05). CONCLUSIONS: MiR-182 inhibits oxidative stress and epithelial cell apoptosis in the lens of cataract rats by activating the PI3K/Akt signaling pathway.