首页> 外文期刊>Natural product communications >Essential Oil from Leaves of Liquidambarformosana Ameliorates Inflammatory Response in Lipopolysaccharide-activated Mouse Macrophages
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Essential Oil from Leaves of Liquidambarformosana Ameliorates Inflammatory Response in Lipopolysaccharide-activated Mouse Macrophages

机译:枫香的叶子精油改善脂多糖激活的小鼠巨噬细胞的炎症反应。

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The essential oil from Liquidambar formosana leaves (EOLF) was demonstrated to exhibit anti-inflammatory activity in mouse macrophages. EOLF reduced nitrite oxide generation, secretion levels of tumor necrosis factor-a and interleukin-6, and expression levels of prointerleukin-1 β, inducible nitric oxide synthase, and cyclooxygenase-2 in lipopolysaccharide (LPS)-activated mouse macrophages. EOLF also reduced NLRP3 inflammasome-derived interleukin-1 β secretion. The underlying mechanisms for the EOLF-mediated anti-inflammatory activity were (1) reduction of LPS-induced reactive oxygen species generation; (2) reduction of LPS-induced activation of c-Jun N-terminal kinase, extracellular signal-regulated kinase, and p38 MAP kinase; (3) reduction of LPS-induced nuclear factor-κB activation. Furthermore, 25 compounds were identified in the EOLF using GC-FID and GC-MS and the major compounds were terpinen-4-ol (32.0%), β-pinene (18.0%), γ-terpinene (13.8%), and α-terpinene (9.7%). We found that LPS-induced nitrite oxide generation was inhibited significantly by terpinen-4-ol. Our results indicated that EOLF has anti-inflammatory activity and may provide a molecular rationale for future therapeutic interventions in immune modulation.
机译:枫香枫叶(EOLF)的精油被证明在小鼠巨噬细胞中表现出抗炎活性。 EOLF减少了脂多糖(LPS)激活的小鼠巨噬细胞中亚硝酸盐的生成,肿瘤坏死因子-a和白细胞介素6的分泌水平以及原白细胞介素1β,诱导型一氧化氮合酶和环加氧酶2的表达水平。 EOLF还减少了NLRP3炎性体来源的白介素1β的分泌。 EOLF介导的抗炎活性的潜在机制是(1)降低LPS诱导的活性氧的产生; (2)减少LPS诱导的c-Jun N末端激酶,细胞外信号调节激酶和p38 MAP激酶的活化; (3)减少LPS诱导的核因子-κB活化。此外,使用GC-FID和GC-MS在EOLF中鉴定出25种化合物,主要化合物为萜品烯-4-醇(32.0%),β-pine烯(18.0%),γ-萜品烯(13.8%)和α -松油烯(9.7%)。我们发现,萜品四醇显着抑制LPS诱导的亚硝酸盐生成。我们的结果表明,EOLF具有抗炎活性,并可能为免疫调节的未来治疗性干预提供分子基础。

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