Metformin Suppresses Inflammation Via AMP-activated Protein Kinase In Glomerular Mesangial Cells In Vitro Of Rat

Methods MCs (Mesangial cells) were incubated in the intermedium of normal concentration glucose (5.6 mmol/L, group NG), high concentration glucose (25mmol/L, group HG) and different concentrations of metformin (group M1,M2, M3). After 48h incubation, the MCs and supernatants were gathered. The expression of NF-κB, MCP-1, ICAM-1, and TGF-β1 mRNA was analyzed by real time polymerase chain reaction. Western blot was used to detect the expression of AMPK, phospho-Thr-172 AMPK(p-AMPK), NF-icBp65, MCP-1, ICAM-1, and TGF-β1 protein.Results After stimulated by HG, the synthesis of NF-κB, MCP-1, ICAM-1, TGF-β1 mRNA and protein in group HG increased significantly compared with group NG (P<0.05). Both genes and protein expression of NF-κB, MCP-1, ICAM-1, TGF-β1 of MCs induced by high glucose were markedly reduced after metformin treatment in a dose-dependent manner (P<0.05). The expression of p-AMPK increasead with the rising of metformin concentration, presenting the opposite trend, while the level of total-AMPK protein was unchanged with exposure to HG or metformin.Conlusions Metformin can suppress the expression of NF-κB, MCP-1, ICAM-1 and TGF-β1 of glomerular MCs induced by high glucose via AMPK activation, which may partly contribute to its reno-protection.