Emodin ameliorates high-glucose induced mesangial p38 over-activation and hypocontractility via activation of PPARgamma.

ABSTRACT: Early stage diabetic nephropathy is characterized by elevated glomerular filtration. Recent studies have identified high-glucose induced p38 MAPK (p38) over-activation in mesangial cells. Mesangial hypocontractility is the major underlying mechanism, however, no ameliorating agents are currently available. We investigated the protective effects of emodin on high-glucose induced mesangial cell hypocontractility. Mesangial cells were cultured under normal (5.6 mM) and high glucose (30 mM) conditions. Emodin was administrated at doses of 50 mg/l and 100 mg/l. Angiotension II stimulated cell surface reductions were measured to evaluate cell contractility. p38 activity was detected using Western blotting. To further explore the possible mechanism of emodin, expression of the peroxisome prolifer

SUBMITTER: Liu Y 

PROVIDER: S-EPMC2753658 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature