The accurate role of ANRIL in cataract is poorly understood. We aimed to reveal the effects of ANRIL on H2O2-treated HLECs, SRA01/04, as well as the regulatory mechanisms. Oxidative stress model of HLECs was induced by H2O2. Cell injury was evaluated according to cell proliferation, apoptosis and DNA damage using CCK-8 assay/flow cytometry and TUNEL assays/γH2AX staining. Expressions of ANRIL and miR-21 in HLECs were determined by RT-qPCR. The effects of miR-21, miR-34a and miR-122-5p inhibition as well as AMPK and β-catenin on HLECs with ANRIL overexpression and H2O2 stimulation were analyzed. In vivo experiment was performed via RT-qPCR. H2O2 repressed proliferation and induced apoptosis or DNA damage in HLECs. Those alterations induced by H2O2 were attenuated by ANRIL overexpression. MiR-21 was positively regulated by ANRIL, and both of them were repressed in H2O2-induced HLECs and cataract patient tissues. Inhibition of miR-21 but not miR-34a or miR-122-5p reversed the effects of ANRIL on H2O2-treated HLECs. Phosphorylation of AMPK and expression of β-catenin were increased by ANRIL via regulating miR-21. AMPK and β-catenin affected beneficial function of ANRIL-miR-21 axis.

Therefore, lncRNA ANRIL attenuated H2O2-induced cell injury in HELCs via up-regulating miR-21 via the activation of AMPK and β-catenin.