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Objective:To study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA).Methods:The changes of prostaglandin E_2(PGE_2),tumor necrosis factor(TNF-α),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-αproduction 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.Conclusion:The anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE_2 are through inhibiting COX-2 mRNA expression without TNF-α changes.
Objective: To study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA). Methods: The changes of prostaglandin E_2 (PGE_2), tumor necrosis factor (TNF-α), 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-αproduction 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). L,P<0.01 vs.LPS),respectively.Conclusion:The anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE_2 are through inhibiting COX-2 mRNA expression without TNF-α changes.