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Myrrh mediates haem oxygenase-1 expression to suppress the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages
被引:17
|作者:
Cheng, Yu-Wen
[2
]
Cheah, Khoot-Peng
[1
]
Lin, Che-Wei
[1
]
Li, Joe-Sharg
[1
]
Yu, Wen-Yu
[1
]
Chang, Ming Long
[1
]
Yeh, Geng-Chang
[3
]
Chen, Sheng-Hsuan
[5
,6
]
Choy, Cheuk-Sing
[1
,4
]
Hu, Chien-Ming
[1
,4
]
机构:
[1] Taipei Med Univ Hosp, Emergency Dept, Taipei 110, Taiwan
[2] Taipei Med Univ, Sch Pharm, Coll Pharm, Taipei, Taiwan
[3] Taipei Med Univ, Sch Med, Dept Pediat, Taipei, Taiwan
[4] Taipei Med Univ, Sch Med, Coll Med, Dept Primary Care Med, Taipei, Taiwan
[5] Taipei Med Univ Hosp, Dept Internal Med, Div Gastroenterol, Taipei 110, Taiwan
[6] Mennonite Christian Hosp, Hualien, Taiwan
关键词:
cyclooxygenase-2;
haem oxygenase-1;
inducible nitric oxide synthase;
lipopolysaccharide;
myrrh;
NF-KAPPA-B;
HUMAN GINGIVAL FIBROBLASTS;
NITRIC-OXIDE;
COMMIPHORA-MOLMOL;
AQUEOUS EXTRACT;
NO PRODUCTION;
ACTIVATION;
GUGGULSTERONE;
INDUCTION;
SESQUITERPENES;
D O I:
10.1111/j.2042-7158.2011.01329.x
中图分类号:
R9 [药学];
学科分类号:
1007 ;
摘要:
Objectives To elucidate a novel anti-inflammatory mechanism of myrrh against lipopolysaccharide (LPS)-induced inflammation. Methods RAW264.7 macrophages were cultured in DMEM and then cells were treated with LPS or LPS plus a myrrh methanol extract (MME) for 24 h. The culture medium was collected for determination of nitric oxide (NO), prostaglandin (PG)E-2, interleukin (IL)-1 beta, and tumour necrosis factor (TNF)-alpha, and cells were harvested by lysis buffer for Western blot analysis. Key findings Our data showed that treatment with the MME (1 similar to 100 mu g/ml) did not cause cytotoxicity or activate haem oxygenase-1 (HO-1) protein synthesis in RAW264.7 macrophages. Furthermore, the MME inhibited LPS-stimulated NO, PGE(2), IL-1 beta and TNF-alpha release and inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 protein expression. Zn(II) protoporphyrin IX, a specific inhibitor of HO-1, blocked the inhibition of iNOS and COX-2 expression by the MME. Conclusions These results suggest that among mechanisms of the anti-inflammatory response, the MME inhibited the production of NO, PGE(2), IL-1 beta and TNF-alpha by downregulating iNOS and COX-2 gene expression in macrophages and worked through the action of HO-1.
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页码:1211 / 1218
页数:8
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