Abstract
Cataracts account for ~50% of the cases of blindness in individuals worldwide. The apoptosis of lens epithelial cells (LECs) occurs during the formation of cataracts, which is a non-congenital condition. Numerous microRNAs (miRs) have been reported to regulate apoptosis in LECs. For instance, miR-23a expression levels were shown to be upregulated in cataractous lenses; however, the function of miR-23a in cataracts remains undetermined. To establish an in vitro model of cataracts, human LECs, HLE-B3 cells, were induced with 200 µmol/l H2O2 for 24 h. HLE-B3 cells were transfected with the miR-negative control (NC) mimic, miR-23a-3p mimic, miR-NC inhibitor, miR-23a-3p inhibitor, small interfering RNA (siRNA) targeting BCL2 (siRNA-BCL2) and siRNA-NC. The expression levels of miR-23a-3p were detected using reverse transcription-quantitative PCR. The interaction between miR-23a-3p and the 3'-untranslated region (UTR) of the target mRNA BCL2 was predicted by TargetScan 7.1, and further validated using a dual luciferase reporter assay. The BCL2 protein expression levels were analyzed using western blotting, cell proliferation was determined using a CCK-8 assay and the levels of cell apoptosis were analyzed using flow cytometric analysis. The results of the present study revealed that the expression levels of miR-23a-3p were significantly upregulated, while the expression levels of BCL2 were significantly downregulated in H2O2-induced HLE-B3 cells compared to untreated control cells. BCL2 was shown to be a target of miR-23a-3p. The miR-23a-3p inhibitor subsequently attenuated H2O2-induced apoptosis and increased the proliferation of HLE-B3 cells, which was partially reversed by siRNA-BCL2. In conclusion, the findings of the current study suggested that the inhibition of miR-23a-3p may attenuate H2O2-induced cataract formation by targeting BCL2, thus providing a novel therapeutic target for the treatment of patients with cataracts in the clinic.