Alisol A inhibits the circ_0001831/miR‐346/LIN28B pathway to ameliorate high glucose‐induced injury of human renal mesangial cells.

Background: Alisol A can ameliorate glucose metabolism disorders, however, there is no data regarding its role in diabetic nephropathy (DN). The present work evaluates the role of Alisol A in DN and the underlying mechanism. Methods: RNA expression of circ_0001831, miR‐346, and lin‐28 homolog B (LIN28B) was detected by qRT‐PCR. Cell viability and proliferation were investigated by MTT assay and EdU assay, respectively. The inflammatory cytokines were examined by ELISAs. Oxidative stress was evaluated by the commercial kits. Protein expression was detected by western blotting. The interactions among circ_0001831, miR‐346, and LIN28B were identified by dual‐luciferase reporter assay and RIP assay. DN mouse model assay was used to analyse the effect of Alisol A on renal injury of diabetic mice. Results: HG treatment promoted HRMC proliferation, fibrosis, inflammation, and oxidative stress; however, these effects were reversed after Alisol A treatment. Alisol A treatment ameliorated STZ‐induced renal injury of diabetic mice. Additionally, circ_0001831 or LIN28B overexpression or miR‐346 downregulation relieved Alisol A‐induced effects under HG conditions. Mechanistically, circ_0001831 acted as a miR‐346 sponge, and LIN28B was identified as a target gene of miR‐346. Further, the regulation of circ_0001831 in HG‐induced HRMC dysfunction involved LIN28B. Conclusion: Alisol A ameliorated HG‐induced HRMC fibrosis, inflammation, and oxidative stress and STZ‐induced renal injury of diabetic mice by regulating the circ_0001831/miR‐346/LIN28B pathway. [ABSTRACT FROM AUTHOR]