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莳萝花提取物通过阻断巨噬细胞中诱导型一氧化氮合酶(iNOS)的表达和核因子κB(NF-κB)的活性,抑制脂多糖诱导的炎症反应。

Anethum graveloens flower extracts inhibited a lipopolysaccharide-induced inflammatory response by blocking iNOS expression and NF-κB activity in macrophages.

作者信息

Kim Yong-Jae, Shin Yusu, Lee Kwang Ho, Kim Tack-Joong

机构信息

Division of Biological Science and Technology, College of Science and Technology, Yonsei University, Wonju, Korea.

出版信息

Biosci Biotechnol Biochem. 2012;76(6):1122-7. doi: 10.1271/bbb.110950. Epub 2012 Jun 7.

Abstract

Inflammation is a system used by a host to defend against the presence of bacteria, viruses, or yeasts. Toll-like receptors (TLRs) in the plasma membranes of macrophages are activated when they recognize the molecular structure of a virus or bacterium. Lipopolysaccharide (LPS), an outer cell-wall component of Gram-negative bacteria, initiates an inflammatory process via TLR4. We investigated the effect of the extract of Anethum graveloens flowers (AGFs) on LPS-mediated inflammation in RAW 264.7 cells. The extract markedly suppressed nitric oxide generation in a concentration-dependent manner in LPS-stimulated RAW 264.7 cells. It inhibited inducible nitric oxide synthase (iNOS) and the mRNA expression of cytokines such as interleukin-1 beta and interleukin-6 in LPS-stimulated RAW 264.7 cells. It also inhibited iNOS protein levels in LPS-stimulated RAW 264.7 cells. In addition, AGF decreased the LPS-induced phosphorylation of mitogen-activated protein kinases in LPS-stimulated RAW 264.7 cells. AGF inhibited the phosphorylation of Akt, an upstream molecule of the nuclear factor kappa B (NF-κB) pathway, and thus inhibited NF-κB activity in LPS-stimulated RAW 264.7 cells. These results suggest that AGF exerts an anti-inflammatory effect in LPS-stimulated RAW 264.7 cells by inhibiting iNOS expression and blocking the NF-κB pathway.

摘要

炎症是宿主用来抵御细菌、病毒或酵母存在的一种系统。巨噬细胞质膜中的Toll样受体(TLR)在识别病毒或细菌的分子结构时被激活。脂多糖(LPS)是革兰氏阴性菌的一种外细胞壁成分,通过TLR4引发炎症过程。我们研究了莳萝花提取物(AGF)对RAW 264.7细胞中LPS介导的炎症的影响。该提取物在LPS刺激的RAW 264.7细胞中以浓度依赖性方式显著抑制一氧化氮的产生。它抑制LPS刺激的RAW 264.7细胞中诱导型一氧化氮合酶(iNOS)以及白细胞介素-1β和白细胞介素-6等细胞因子的mRNA表达。它还抑制LPS刺激的RAW 264.7细胞中iNOS蛋白水平。此外,AGF降低了LPS刺激的RAW 264.7细胞中丝裂原活化蛋白激酶的LPS诱导的磷酸化。AGF抑制核因子κB(NF-κB)途径的上游分子Akt的磷酸化,从而抑制LPS刺激 的RAW 264.7细胞中的NF-κB活性。这些结果表明,AGF通过抑制iNOS表达和阻断NF-κB途径在LPS刺激的RAW 264.7细胞中发挥抗炎作用。

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