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芝麻酚通过抑制核因子-κB 的激活来下调脂多糖诱导的炎症反应。

Sesamol down-regulates the lipopolysaccharide-induced inflammatory response by inhibiting nuclear factor-kappa B activation.

机构信息

Department of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.

出版信息

Innate Immun. 2010 Oct;16(5):333-9. doi: 10.1177/1753425909351880. Epub 2009 Nov 25.

Abstract

We examined the effects of sesamol on the lipopolysaccharide (LPS)-induced inflammatory response. Sesamol inhibited serum tumor necrosis factor (TNF)-α, interleukin (IL)-1β and nitrite production in LPS-treated mice, and inhibited LPS-induced inducible nitric oxide synthase expression in mouse leukocytes. Sesamol also down-regulated TNF-α, IL-1β, and nitrite production as well as inducible nitric oxide synthase expression in LPS-treated RAW 264.7 cells. Further, sesamol inhibited LPS-induced nuclear factor (NF)-κB translocation and inhibitor (I)κB-α phosphorylation in RAW 264.7 cells. By inhibiting TNF-α, IL-1β, and nitrite levels, and interfering with the NFκB pathway, sesamol down-regulated the LPS-initiated inflammatory response.

摘要

我们研究了芝麻酚对脂多糖(LPS)诱导的炎症反应的影响。芝麻酚抑制 LPS 处理的小鼠血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和亚硝酸盐的产生,并抑制 LPS 诱导的小鼠白细胞中诱导型一氧化氮合酶的表达。芝麻酚还下调 LPS 处理的 RAW 264.7 细胞中 TNF-α、IL-1β、亚硝酸盐的产生以及诱导型一氧化氮合酶的表达。此外,芝麻酚抑制 LPS 诱导的 RAW 264.7 细胞中核因子(NF)-κB 易位和抑制(I)κB-α磷酸化。通过抑制 TNF-α、IL-1β和亚硝酸盐水平,并干扰 NFκB 途径,芝麻酚下调 LPS 引发的炎症反应。

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