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新木姜子精油通过抑制NF-κB和MAPK激活减轻LPS诱导的RAW 264.7巨噬细胞炎症反应。

Neolitsea sericea essential oil attenuates LPS-induced inflammation in RAW 264.7 macrophages by suppressing NF-kappaB and MAPK activation.

作者信息

Yoon Weon-Jong, Moon Ji-Young, Kang Ji-Yong, Kim Gi-Ok, Lee Nam Ho, Hyun Chang-Gu

机构信息

Jeju High-Tech Development Institute (HiDI), Jeju 699-943, Korea.

出版信息

Nat Prod Commun. 2010 Aug;5(8):1311-6.

Abstract

The chemical composition and anti-inflammatory activities of hydrodistilled essential oil from Neolitsea sericea leaves (NSE) have been investigated for the first time. The chemical constituents of NSE were analysed by GC-MS and found to include sericenine (32.3%), sabinene (21.0%), trans-beta-ocimene (13.3%), beta-caryophyllene (4.8%), and 4-terpineol (4.2%). The effects of NSE on nitric oxide (NO), prostaglandin E2 (PGE2), tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 production in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages were also examined. Pro-inflammatory cytokine and mediator tests indicated that NSE has excellent dose-dependent inhibitory activities. To further examine the mechanism responsible for the inhibition of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression by NSE, we examined the effect of NSE on nuclear factor-kappaB (NF-kappaB) activation and the phosphorylation of mitogen-activated protein kinases (MAPK). NSE inhibited NF-kappaB activation by LPS, and this was associated with the abrogation of IkappaB-alpha phosphorylation and subsequent decreases in nuclear p50 and p65 protein levels. Further, the phosphorylation of p38, ERK and JNK was suppressed by NSE in a concentration-dependent manner. These results suggest that NSE exerts anti-inflammatory effects in LPS-stimulated RAW 264.7 macrophages by inhibition of NF-kappaB activation and MAPK phosphorylation, and, therefore, may be useful for treatment of inflammatory diseases.

摘要

首次对新木姜子叶水蒸馏精油(NSE)的化学成分和抗炎活性进行了研究。通过气相色谱 - 质谱联用仪(GC - MS)分析了NSE的化学成分,发现其包含绢毛木姜子碱(32.3%)、桧烯(21.0%)、反式-β-罗勒烯(13.3%)、β-石竹烯(4.8%)和4 - 松油醇(4.2%)。还检测了NSE对脂多糖(LPS)激活的RAW 264.7巨噬细胞中一氧化氮(NO)、前列腺素E2(PGE2)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL - 6产生的影响。促炎细胞因子和介质测试表明,NSE具有出色的剂量依赖性抑制活性。为了进一步研究NSE抑制诱导型一氧化氮合酶(iNOS)和环氧化酶 - 2(COX - 2)表达的机制,我们检测了NSE对核因子 - κB(NF - κB)激活和丝裂原活化蛋白激酶(MAPK)磷酸化的影响。NSE抑制LPS诱导的NF - κB激活,这与IκB - α磷酸化的消除以及随后核p50和p65蛋白水平的降低有关。此外,NSE以浓度依赖性方式抑制p38、ERK和JNK的磷酸化。这些结果表明,NSE通过抑制NF - κB激活和MAPK磷酸化在LPS刺激的RAW 264.7巨噬细胞中发挥抗炎作用,因此可能对炎症性疾病的治疗有用。

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