Chinese journal of integrative medicine 2009;15(3):210-215

doi:10.1007/s11655-009-0210-0

Anti-inflammatory mechanism of total glycosides of Acanthopanax Giraldii.

Fang YUAN 1 ; Jie CHEN ; Guo-min XU ; Jia-jia ZHENG ; Qi-cai LONG

Affiliations

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Country

China

Language

English

MeSH

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.