β‐Amyrin ameliorates diabetic nephropathy in mice and regulates the miR‐181b‐5p/HMGB2 axis in high glucose‐stimulated HK‐2 cells

• DOI: 10.1002/tox.23431
• Publication Date: 2021-12-11T09:05:07Z
• Authors: Wenhua Xu; Hongwu Zhang; Qinfeng Zhang; Jialan Xu
• Keywords: Viability assay

Diabetic nephropathy (DN) is a diabetic complication that can cause renal failure. β-amyrin has been identified to possess anti-diabetic property. This study was designed evaluate the potential role of in DN and its underlying mechanism. Streptozotocin-induced mice were used as vivo model, high glucose (HG)-stimulated human proximal tubular HK-2 cells utilized vitro model. Renal histological changes assessed by hematoxylin-eosin periodic acid-Schiff staining. cell viability apoptosis detected Cell Counting Kit-8 assay flow cytometry analysis, respectively. found ameliorate kidney injury suppressed inflammatory response well HG-stimulated cells. miR-181-5p expression murine tissues situ hybridization (ISH) fluorescence (FISH). MiR-181b-5p, previously target for disease, downregulated HG stimulated cells, induced upregulation miR-181b-5p. Binding relationship between miR-181b-5p mobility group box 2 (HMGB2) confirmed luciferase reporter assay. MiR-181b-5p bound 3' untranslated region HMGB2 suppress expression. As shown immunohistochemical staining immunofluorescence staining, upregulated models DN, downregulation HMGB2. Moreover, overexpression neutralized suppressive effects elevation on HG-treated Overall, ameliorates suppresses via miR-181b-5p/HMGB2 axis.