PPAR-γ is involved in the protective effect of 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside against cardiac fibrosis in pressure-overloaded rats.

2, 3, 4', 5-tetrahydroxystilbene-2-0-ß-D glucoside (TSG) could inhibit cardiac remodeling in response to pressure overload. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has been recognized as a potent, endogenous antifibrotic factor and maintaining a proper expression level in myocardium is necessary for assuring that structure and function of heart adapt to pressure overload stress. The aim of the present study was to investigate whether PPAR-γ is involved in the beneficial effect of TSG on pressure overload-induced cardiac fibrosis. TSG (120mg/kg/day) or TSG (120mg/kg/day) plus the PPAR-γ antagonist GW9662 (1mg/kg/day) was administered to rats with pressure overload induced by abdominal aortic banding. 30 days later, pressure overload-induced hypertension, cardiac dysfunction and fibrosis were significantly inhibited by TSG. TSG also significantly reduced collagen I, collagen III, fibronectin and plasminogen activator inhibitor (PAI)-1 expression, as makers of myocardial fibrosis. Theses anti-fibrotic effects of TSG in pressure overloaded hearts could be abrogated by co-treatment with GW9662. Accordingly, upregulated PPAR-γ protein expression by TSG in pressure overloaded hearts was also reversed by co-treatment with GW9662. Additionally, the inhibitory effects of TSG on angiotensin II induced cardiac fibroblasts proliferation, differentiation and expression of collagen I and III, fibronectin and PAI-1 were abrogated by PPAR-γ antagonist GW9662 and PPAR-γ silencing. Furthermore, TSG directly increased PPAR-γ gene expression at gene promoter, mRNA and protein level in angiotensin II-treated cardiac fibroblats in vitro. Our results suggested that upregualtion of endogenous PPAR-γ expression by TSG may be involved in its beneficial effect on pressure overload-induced cardiac fibrosis.

[Study on the mechanism by which Rhubarb protects the mucosal barrier of intestine of mouse].

OBJECTIVE: To observe the influence of Rhubarb on the the excretion of Type II PLA2 and lysozyme of small intestine of mouse. METHODS: Forty ICR mice were randomized to two groups. In the experiment group, the mice were gavaged with 0.3 ml 10% Rhubarb decoction every 8 hours; in the control group, the mice were given normal saline instead of Rhubarb decoction. After 24 hours, the mice were subjected to cervical dislocation, and their jejunum and ileum were taken out. The lumen of each resected intestine was rinsed with 100 g/L acetic acid, and the washed intestines from each mouse were cut into pieces 1-2 mm in length. Then the perfusate and homogenate were prepared, lyophilized, sealed, and stored at -20 degrees C. The Type II PLA2 activity and lysozyme were assayed respectively. RESULTS: The Type II PLA2 activities and lysozyme of homogenate in Rhubarb group were lower than those in Saline group (P<0.01). The type II PLA2 activities and lysozyme of perfusate in Rhubarb group were higher than those in Saline group (P<0.01). CONCLUSION: Rhubarb can stimulate the small intestine of mice to excrete Type II PLA2 and lysozyme, thus resulting in the increase of Type II PLA2 and lysozyme contents in the intestinal tract and enhancing the function of mucosal barrier of intestine.