Effects of emodin on TGF-β1/ERK1/2 and FN protein expression in rat glomerular mesangial cells induced by high glucose

Objective To investigate the effects of emodin (EMO) on the TGF-β1/ERK1/2, extracellular matrix (ECM) and FN protein in rat glomerular mesangial cells (MCs) induced by high glucose. MethodsMCs were divided into four groups: a normal control group (NG, 5.56 mmol/L glucose), a mannitol group (MA, 5.56 mmol/L+24.44 mmol/L mannitol), a solvent group (0.1%DMSO+30 mmol/L glucose), a high glucose group (HG, 30 mmol/L glucose) and an Emodin intervention group (1 μmol/L, 10 μmol/L EMO+30 mmol/L glucose). The cell proliferation was measured by CCK-8 assay. The levels of TGF-β1, p-ERK1/2 and FN were detected by Western blotting. ResultsCompared with the NG group, the HG group presented obvious proliferation after cultivation for 48 h (P<0.05 or P<0.01) and produced significantly increased levels of p-ERK1/2, TGF-β1 and FN (P<0.05). Compared with the HG group, the Emodin intervention group showed suppressed proliferation and remarkably reduced levels of p-ERK1/2, TGF-β1, and FN (P<0.05 or P<0.01). ConclusionsEmodin can inhibit the proliferation of MCs induced by high glucose and down-regulate the levels of p-ERK1/2, TGF-β1 and FN, which plays a role in the prevention and treatment of diabetic nephropathy.