LAUSR

Abstract Objective Renal failure is very common in Diabetic nephropathy (DN) at terminal stage. Long-chain non-coding RNA (LncRNA) improves DN by regulating microRNA (miR). In this study, we investigate the role of MALAT1/miR-206 on high glucose (HG)-induced inflammation, oxidative stress and cell death of renal tubular epithelial cells (RTECs) in Diabetic nephropathy (DN). Methods DN cell model was established by treating HK‐2 cells with high glucose (HG) in vitro. Transfection effect was confirmed by qRT-PCR and MALAT1, NLRP3, Caspase-1, IL-1β, GSMDD-N and miR-206 were tested. Western blot was performed to test the proteins in NLRP3, Caspase-1, IL-1β and GSMDD-N, and to observe the pyroptosis. Elisa kit was applied to detect TNF-α, IL-6 and MCP-1. MALAT1, miR‐206, and NLRP3 were examined via dual‐luciferase reporter assay to established co relation among these factors. Results Double luciferase report experiment and RNA immunoprecipitation (RIP) confirmed that MALAT1 could bind to miR-206. HG induced MALAT1 in HK-2 cells increased. Knocking down MALAT1 could reduce TNF-α, IL-6 and MCP-1. In HG-intervened HK-2 cells, the over-expressed miR-206 transfected into the cells was consistent with the changes of inflammatory factors and cytokines after knock-down MALAT1. Conclusion Up-regulation MALAT1 could reverse the inhibition of miR-206 on pyroptosis and inflammatory response. MALAT1 can improve HG-induced HK-2 pyroptosis by targeting miR-206, which is expected to be a latent target to treat DN in clinic.