Myrrh mediates haem oxygenase-1 expression to suppress the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages

被引:19
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
100702 [药剂学];
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.
引用
收藏
页码:1211 / 1218
页数:8
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