The effect of Ginkgo biloba extract on portal hypertension and hepatic microcirculation in rats.
- Author:
Chun-qing ZHANG
1
;
Yu-hua ZHU
;
Jing WANG
;
Bin LIANG
;
Hong-wei XU
;
Cheng-yong QIN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Ginkgo biloba; Hepatic Veins; pathology; Hypertension, Portal; drug therapy; physiopathology; Liver Cirrhosis, Experimental; chemically induced; drug therapy; pathology; physiopathology; Male; Microcirculation; drug effects; Plant Extracts; pharmacology; Rats; Rats, Wistar
- From: Chinese Journal of Hepatology 2007;15(4):245-248
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the effect of Ginkgo biloba extract (EGb) on hepatic microcirculation and portal hypertension in CCl4 treated rats.
METHODSTwenty-five male Wistar rats were divided into a blank, a CCl4 treated and a CCl4 plus EGb treated group, and all were treated for 10 weeks. The free portal vein pressures were measured through catheterizations. Hepatic sinusoidal endothelial cells and other parameters of hepatic microcirculation were studied with transmission electron microscopy. The amounts of malondialdehyde (MDA), endothelin (ET-1), platelet-activating factor (PAF), nitric oxide (NO), cNOS and iNOS in the liver tissues were determined.
RESULTSThe portal vein pressure of the CCl4 plus EGb treated group was (7.4 +/- 0.6) mm Hg while the pressure of the CCl4 treated group was (8.7 +/- 0.8) mm Hg. Aggregation of blood cells or microthrombosis in hepatic sinusoids, deposition of collagen in hepatic sinusoids and spaces of Disse, injury of endothelial cells and capillarization of hepatic sinusoid were significantly milder in the EGb group. The amounts of MDA, ET-1, PAF, NO and iNOS were markedly lower in the CCl4 plus EGb treated group than in the CCl4 treated group.
CONCLUSIONThe results demonstrated that EGb can decrease the portal vein pressure and improve hepatic microcirculation in CCl4 treated rats. The mechanisms of this effect may involve its inhibition on ET-1, PAF, lipid peroxidation, and down regulation of the hepatic iNOS and NO expressions.