지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2006.9
- 수록면
- 293 - 299 (7page)
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초록· 키워드
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We demonstrate that magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells (murine macrophage cell line). Treatment of RAW 264.7 cells with magnolol inhibited LPS-stimulated nitric oxide production in a dose-related manner. RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression. Western immunoblot analysis of phosphorylate p38 kinase showed magnolol significantly inhibited the phosphorylation of p38 kinase which is important in the regulation of iNOS gene expression. The specific p38 inhibitor SB203580 abrogated the LPSinduced NO generation and iNOS expression, whereas the selective MEK-1 inhibitor PD98059 did not affect the NO induction. Immunostaining of p65 and reporter gene assay showed that magnolol inhibited NF-κ/Rel nuclear translocation and transcriptional activation, respectively. Collectively, this series of experiments indicates that magnolol inhibits iNOS gene expression by blocking NF-κ/Rel and p38 kinase signaling. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of magnolol on iNOS suggest that magnolol may represent a useful anti-inflammatory agent.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-513-017426745