Protective effects and its mechanisms of total alkaloids from rhizoma Coptis chinensis on Helicobacter pylori LPS induced gastric lesion in rats.
- Author:
Jin-song LU
1
;
Yu-qing LIU
;
Ming LI
;
Bao-sheng LI
;
Yan XU
Author Information
- Publication Type:Journal Article
- MeSH: Acute Disease; Alkaloids; isolation & purification; pharmacology; Animals; Apoptosis; drug effects; Coptis; chemistry; Epithelial Cells; drug effects; enzymology; pathology; Gastric Mucosa; drug effects; enzymology; pathology; Gastritis; blood; chemically induced; prevention & control; Lipopolysaccharides; Male; Nitric Oxide Synthase Type II; metabolism; Nitric Oxide Synthase Type III; metabolism; Plants, Medicinal; chemistry; Protective Agents; isolation & purification; pharmacology; Rats; Rats, Sprague-Dawley; Rhizome; chemistry; Tumor Necrosis Factor-alpha; blood
- From: China Journal of Chinese Materia Medica 2007;32(13):1333-1336
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects and its possible mechanisms of total alkaloids (TA) from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats.
METHODH. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100, 200 mg x kg(-1) TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-alpha and the gastric mucus epithelial cell apoptosis.
RESULTH. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-alpha in serum. Treatment with 50, 100, 200 mg x kg(-1) TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-alpha in serum, decline in NOS-2, and increase in cNOS.
CONCLUSIONThe findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammation. The concerned mechanisms may be related to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregulating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-alpha.
