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Abstract: Objective To explore the effect of miR-30b-3p on HK-2 cell proliferation, apoptosis and oxidative stress induced by sodium oxalate and the mechanism by targeting ZNRF1. Methods HK-2 cells were treated with 0. 2 μmol / L or 0. 6 μmol / L sodium oxalate. miR-30b-3p mimic and miR-30b-3p inhibitor and their corresponding control were transfected into HK-2 cells. The proliferation, invasion and migration of HK-2 cells were detected by CCK-8, transwell and wound-healing assay, respectively. Intracellular ROS was measured by flow cytometry. The activities of LDH, MDA and GSH were detected by ELISA. The expression levels of Bax and Bcl-2 were analyzed by Western blotting. Luciferase gene reporter assay was used to verify the targeting relationship between miR-30b-3p and ZNRF1. The relationship between miR-30b-3p and ZNRF1 was analyzed by RNA immunoprecipitation. Results  Sodium oxalate treatment significantly increased ROS, LDH and MDA levels and decreased GSH levels in HK-2 cells (P< 0. 01). Sodium oxalate also inhibited the proliferation, migration and invasion, and promoted apoptosis of HK-2 cells. miR-30b-3p promoted the effect of sodium oxalate on HK-2 cells. The results of gene target prediction and luciferase assay indicated that ZNRF1 is a direct target of miR-30b-3p in HK-2 cells, and ZNRF1 silencing reversed the effect of miR-30b-3p on sodium oxalate induced HK-2 cell damage. Conclusion miR-30b-3pcan promote the apoptosis and oxidative stress induced by sodium oxalate in HK-2 cells, and inhibitcell proliferation, invasion and migrationvia ZNRF1.

Key words: miR-30b-3p, ZNRF1, sodium oxalate, HK-2, oxidative stress