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蛇菰宁,一种来自蛇菰属的木脂素,通过抑制 c-raf/MEK1/2/ERK 1/2 通路的激活来减少肿瘤坏死因子-α的产生。

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.

机构信息

Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School, 8 Hak-dong, Gwangju 501-746, Korea.

出版信息

Int Immunopharmacol. 2010 Sep;10(9):1022-8. doi: 10.1016/j.intimp.2010.06.001. Epub 2010 Jun 23.

Abstract

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.

摘要

我们研究了从中华蛇菰中分离得到的木脂素化合物 sauchinone 的抗炎作用及其在脂多糖 (LPS) 刺激的 RAW264.7 细胞中的作用机制。为了评估 sauchinone 对 LPS 诱导的巨噬细胞活化的影响,我们测量了肿瘤坏死因子 (TNF)-α和巨噬细胞炎症蛋白 (MIP)-2 的产生,以及丝裂原活化蛋白激酶 (MAPKs),包括细胞外信号调节激酶 (ERK) 1/2、c-Jun 氨基末端激酶和 p38 丝裂原活化蛋白激酶,以及 LPS 刺激的 RAW264.7 细胞中 NF-κB 的激活。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 的激活。我们的结果表明,sauchinone 通过抑制 ERK1/2 通路抑制 NF-κB 激活,从而抑制巨噬细胞中 LPS 诱导的 TNF-α表达,这可能构成了 sauchinone 的抗炎作用。

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