Anti-inflammatory mechanism of total glycosides of Acanthopanax Giraldii.
- Author:
Fang YUAN
1
;
Jie CHEN
;
Guo-min XU
;
Jia-jia ZHENG
;
Qi-cai LONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Anti-Inflammatory Agents; pharmacology; Cell Line; Cyclooxygenase 1; genetics; Cyclooxygenase 2; genetics; Dinoprostone; metabolism; Drugs, Chinese Herbal; pharmacology; Eleutherococcus; Female; Gene Expression Regulation, Enzymologic; drug effects; Glycosides; pharmacology; Lipopolysaccharides; pharmacology; Macrophages, Peritoneal; cytology; drug effects; metabolism; Mice; Mice, Inbred BALB C; Nitric Oxide; metabolism; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese journal of integrative medicine 2009;15(3):210-215
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA).
METHODSThe changes of prostaglandin E(2)(PGE(2)), tumor necrosis factor (TNF-alpha), nitric oxide (NO), and expressions of COX-1 mRNA and COX-2 mRNA in BALB/c mouse macrophages were observed by the radioimmunoassay, ELISA and nitric acid reduction and RT-PCR in the presence or absence of TGA.
RESULTS(1) TGA could significantly decrease the production of PGE(2)and NO in mouse peritoneal macrophages. The inhibitory rate to LPS-induced PGE(2)production was 87% (TGA 100 mg/L, P<0.05, vs. LPS) and 62% (TGA 20 mg/L, P<0.05, vs. LPS), respectively. The inhibitory rate of NO production in mouse peritoneal macrophages was 49% (TGA 100 mg/L, P<0.05, vs. LPS) and 21% (TGA 20 mg/L, P<0.05 vs. LPS), respectively. TGA could not inhibit LPS-induced TNF-alpha production in mouse peritoneal macrophages. (2) TGA also inhibited the expression of COX-1 and COX-2 mRNA in RAW264.7 cells. The inhibitory rate of TGA to COX-1 mRNA was 22% (TGA 100 mg/L, P<0.05, vs. blank). The inhibitory rate of TGA to COX-2 mRNA was 55% (TGA 20 mg/L, P<0.05, vs. LPS) and 100% (TGA 100 mg/L, P<0.01 vs. LPS), respectively.
CONCLUSIONThe anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE(2)are through inhibiting COX-2 mRNA expression without TNF-alpha changes.
