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首页> 外文期刊>International immunopharmacology >Sauchinone, a lignan from Saururus chinensis, reduces tumor necrosis factor-alpha production through the inhibition of c-raf/MEK1/2/ERK 1/2 pathway activation.
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Sauchinone, a lignan from Saururus chinensis, reduces tumor necrosis factor-alpha production through the inhibition of c-raf/MEK1/2/ERK 1/2 pathway activation.

机译:绍龙属的木脂素Sauchinone通过抑制c-raf / MEK1 / 2 / ERK 1/2途径的活化来减少肿瘤坏死因子-α的产生。

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摘要

We investigated the anti-inflammatory effects of sauchinone, a lignan isolated from Saururus chinensis, and the underlying mechanism in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. To assess the effects of sauchinone on LPS-induced macrophages activation, we measured the production of tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP)-2, and activation of mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) 1/2, c-Jun amino terminal kinases and p38 mitogen-activated protein kinase, and NF-kappaB activation in RAW264.7 cells. Sauchinone decreased the production of TNF-alpha, but not MIP-2 production in RAW264.7 cells stimulated with LPS. Sauchinone also decreased c-Raf-MEK1/2-ERK1/2 phosphorylation and NF-kappaB activation in RAW264.7 cells stimulated with LPS. Our results show that sauchinone inhibits LPS-induced TNF-alpha expression in macrophages by suppression of NF-kappaB activation via ERK1/2 pathway, which may constitute anti-inflammatory effects of sauchinone.
机译:我们调查了从金龙属中分离出的木脂素sauchinone的抗炎作用以及脂多糖(LPS)刺激的RAW264.7细胞的潜在机制。为了评估sauchinone对LPS诱导的巨噬细胞激活的影响,我们测量了肿瘤坏死因子(TNF)-α和巨噬细胞炎性蛋白(MIP)-2的产生,以及丝裂原激活的蛋白激酶(MAPK)的激活,包括细胞外信号RAW264.7细胞中可调节的激酶(ERK)1/2,c-Jun氨基末端激酶和p38丝裂原活化的蛋白激酶以及NF-κB活化。 Sauchinone降低了LPS刺激的RAW264.7细胞中TNF-α的产生,但不降低MIP-2的产生。 Sauchinone还降低了LPS刺激的RAW264.7细胞中c-Raf-MEK1 / 2-ERK1 / 2磷酸化和NF-κB活化。我们的结果表明,sauchinone通过抑制经由ERK1 / 2途径的NF-κB活化来抑制巨噬细胞中LPS诱导的TNF-α表达,这可能构成了sauchinone的抗炎作用。

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