Protective effect of panax japonics on ethanol-induced mice gastric lesion.
- Author:
You-Gui LI
1
;
Gang XU
;
Shi CHEN
;
Shi ZHONG
;
Dong-Feng JI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Catalase; blood; metabolism; Drugs, Chinese Herbal; isolation & purification; pharmacology; therapeutic use; Ethanol; Gastric Mucosa; drug effects; metabolism; pathology; Glutathione; blood; metabolism; Glutathione Peroxidase; blood; metabolism; Male; Malondialdehyde; blood; metabolism; Mice; Mice, Inbred ICR; Microscopy, Electron; Mitochondria; drug effects; ultrastructure; Panax; chemistry; Phytotherapy; Plants, Medicinal; chemistry; Protective Agents; isolation & purification; pharmacology; therapeutic use; Random Allocation; Stomach Diseases; blood; chemically induced; prevention & control
- From: China Journal of Chinese Materia Medica 2007;32(21):2282-2285
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the protective effects of Panax japonics (PJ) on alcohol-induced gastric lesion in mice and the possible mechanisms.
METHODMale ICR mice were randomized into six groups: normal, control, PJ (1.5, 3.0, 6.0 g x kg(-1)) and Yinduoan (1.5 g x kg(-1)). The mice were pretreated with PJ before administering ethanol to observe the effect on the concentration of ethanol in serum and urine. The contents of MDA, GSH and GSH-PX, CAT and SOD activities were measured in serum and gastric mucosa, and subsequently, the pathological evaluation of stomach was also observed.
RESULTThe concentration of ethanol in serum was evidently decreased after PJ (1.5, 3.0 g x kg(-1)) was administrated because the ethanol was eliminated fleetly through urine. Synchronously the PJ reduced the content of MDA and increased the GSH increased in serum and gastric, besides, it increased the enzymatic activities of GSHPX, CAT and SOD, and the ethanol-induced gastric mitochondria structure injury were ameliorated so as to make the function to normal.
CONCLUSIONBased on these observations, one could conclude that the PJ is a potent protective agent against ethanol-induced gastric damages. One mechanism may be related with inhibiting the absorbability of ethanol at gastrointestinal tract, decreasing the concentration of ethanol in serum, and accelerating the ethanol elimination through urine so as to alleviate the ethanol-induced damage to gastrointestinal mucosal, enhancing the first-pass metabolism in stomach, and particularly increasing the antioxidant levels in serum and gastric. These gastroprotective effects might be, at least partly, through ameliorating the gastric mitochondria structure.