Yuan, F., Chen, J., Xu, Gm. et al. Anti-Inflammatory mechanism of total glycosides of Acanthopanax Giraldii., Chin. J. Integr. Med. 15, 210–215 (2009). https://doi.org/10.1007/s11655-009-0210-0
Fang Yuan, Jie Chen, Guo-min Xu, et al. Anti-Inflammatory mechanism of total glycosides of Acanthopanax Giraldii[J]. Chinese Journal of Integrative Medicine, 2009,15(3):210-215.
Yuan, F., Chen, J., Xu, Gm. et al. Anti-Inflammatory mechanism of total glycosides of Acanthopanax Giraldii., Chin. J. Integr. Med. 15, 210–215 (2009). https://doi.org/10.1007/s11655-009-0210-0DOI:
Fang Yuan, Jie Chen, Guo-min Xu, et al. Anti-Inflammatory mechanism of total glycosides of Acanthopanax Giraldii[J]. 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
摘要
To study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA). The changes of prostaglandin E2(PGE2)
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. (1) TGA could significantly decrease the production of PGE2and NO in mouse peritoneal macrophages. The inhibitory rate to LPS-induced PGE2production 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-α 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. The anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE2are through inhibiting COX-2 mRNA expression without TNF-α changes.
Abstract
To study the anti-inflammatory mechanisms of total glycosides of Acanthopanax Giraldii (TGA). The changes of prostaglandin E2(PGE2)
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. (1) TGA could significantly decrease the production of PGE2and NO in mouse peritoneal macrophages. The inhibitory rate to LPS-induced PGE2production 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-α 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. The anti-inflammatory mechanisms of TGA for inhibiting the production of NO and PGE2are through inhibiting COX-2 mRNA expression without TNF-α changes.
关键词
total glycosides of Acanthopanax Giraldiiprostaglandin E2Nitric Oxidetumor necrosis factorCOX mRNA
Keywords
total glycosides of Acanthopanax Giraldiiprostaglandin E2Nitric Oxidetumor necrosis factorCOX mRNA
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相关机构
Institute of Pharmacology and Toxicology, Faculty of Medicine in Pilsen, Charles University, Pilsen, Czech Republic
Department of Pharmacology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences
Department of Hematology, the Affiliated Hospital of Guiyang Medical College
Key Laboratory of Basic Pharmacology of Guizhou and Department of Pharmacology, Zunyi Medical College