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

Yu Wen Cheng, Khoot Peng Cheah, Che-Wei Lin, Joe Sharg Li, Wen Yu Yu, Ming Long Chang, Geng Chang Yeh, Sheng-Hsuan Chen, Cheuk-Sing Choy, Chien-Ming Hu

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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)-1β, and tumour necrosis factor (TNF)-α, and cells were harvested by lysis buffer for Western blot analysis. Key findings Our data showed that treatment with the MME (1∼100 μg/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-1β and TNF-α 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-1β and TNF-α by downregulating iNOS and COX-2 gene expression in macrophages and worked through the action of HO-1.

Original languageEnglish
Pages (from-to)1211-1218
Number of pages8
JournalJournal of Pharmacy and Pharmacology
Volume63
Issue number9
DOIs
Publication statusPublished - Sep 2011

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Heme Oxygenase (Decyclizing)
Methanol
Lipopolysaccharides
Macrophages
Nitric Oxide Synthase Type II
Cyclooxygenase 2
Prostaglandins E
Interleukin-1
Nitric Oxide
Tumor Necrosis Factor-alpha
Anti-Inflammatory Agents
Culture Media
Buffers
Proteins
Down-Regulation
Western Blotting
Inflammation
Gene Expression

Keywords

  • cyclooxygenase-2
  • haem oxygenase-1
  • inducible nitric oxide synthase
  • lipopolysaccharide
  • myrrh

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

Cite this

Myrrh mediates haem oxygenase-1 expression to suppress the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages. / Cheng, Yu Wen; Cheah, Khoot Peng; Lin, Che-Wei; Li, Joe Sharg; Yu, Wen Yu; Chang, Ming Long; Yeh, Geng Chang; Chen, Sheng-Hsuan; Choy, Cheuk-Sing; Hu, Chien-Ming.

In: Journal of Pharmacy and Pharmacology, Vol. 63, No. 9, 09.2011, p. 1211-1218.

Research output: Contribution to journalArticle

Cheng, Yu Wen ; Cheah, Khoot Peng ; Lin, Che-Wei ; Li, Joe Sharg ; Yu, Wen Yu ; Chang, Ming Long ; Yeh, Geng Chang ; Chen, Sheng-Hsuan ; Choy, Cheuk-Sing ; Hu, Chien-Ming. / Myrrh mediates haem oxygenase-1 expression to suppress the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages. In: Journal of Pharmacy and Pharmacology. 2011 ; Vol. 63, No. 9. pp. 1211-1218.
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AU - Li, Joe Sharg

AU - Yu, Wen Yu

AU - Chang, Ming Long

AU - Yeh, Geng Chang

AU - Chen, Sheng-Hsuan

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AB - 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)-1β, and tumour necrosis factor (TNF)-α, and cells were harvested by lysis buffer for Western blot analysis. Key findings Our data showed that treatment with the MME (1∼100 μg/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-1β and TNF-α 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-1β and TNF-α by downregulating iNOS and COX-2 gene expression in macrophages and worked through the action of HO-1.

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