Effect of salvianolic acid B on high glucose-induced phenotypic transition and extracellular matrix secretion in human glomerular mesangial cells
10.3969/j.issn.1000-4718.2019.02.010
- VernacularTitle:丹酚酸B对高糖诱导的肾小球系膜细胞表型转化及细胞外基质分泌的影响
- Author:
Yuan-Mei ZHU
1
;
Bu-Jin YIN
;
Xu ZHANG
;
Bao-Lu TANG
;
Yu-Peng CHENG
;
Jie-Ren YANG
;
Shu-Guo ZHENG
Author Information
1. 皖南医学院药理学教研室
- Keywords:
Salvianolic acid B;
Diabetic nephropathy;
Glomerular mesangial cells;
Phenotypic transition;
Extracellular matrix
- From:
Chinese Journal of Pathophysiology
2019;35(2):248-252
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of salvianolic acid B (Sal B) on high glucose-induced phenotypic transition and extracellular matrix (ECM) secretion in human glomerular mesangial cells (HGMCs) and the underlying mechanisms.METHODS:HGMCs were randomly divided into control group, high glucose group and high glucose plus high dose, medium dose and low dose of Sal B groups.The HGMCs except those in control group were exposed to high glucose (33.3 mmol/L) for 72 h, while those in Sal B groups were co-incubated with indicated concentrations of Sal B.The protein levels ofα-smooth muscle actin (α-SMA) , transforming growth () and phosphorylated Smad2 and p38 mitogen-activated protein kinase (MAPK) were determined by Western blot.The secretion levels of collagen type I (Col I) , collagen type III (Col III) , fibronectin (FN) and laminin (LN) were measured by ELISA.RESULTS:Exposure to high glucose markedly increased the protein expression ofI, Col III, FN and LN in the HG-MCs (P<0.01).The phosphorylation levels of Smad2 and p38 MAPK were also significantly increased (P<0.01).Coincubation with Sal B evidently decreased the protein expression ofI, Col III, FN and LN in the HGMCs induced by high glucose (P<0.05 or P<0.01).The phosphorylated levels of Smad2 and p38 MAPK were also reduced noticeably (P<0.05 or P<0.01).CONCLUSION:Sal B significantly suppresses high glucose-induced phenotypic transition and ECM secretion in the HGMCs, which might be attributed, at least partly, to inhibition ofSmad signaling pathway and p38 MAPK activation.
