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加味四妙散提取物抑制脂多糖刺激的小鼠巨噬细胞释放炎症介质。

Modified Si-Miao-San extract inhibits the release of inflammatory mediators from lipopolysaccharide-stimulated mouse macrophages.

机构信息

Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, PR China.

出版信息

J Ethnopharmacol. 2010 May 4;129(1):5-9. doi: 10.1016/j.jep.2010.02.002. Epub 2010 Feb 20.

DOI:10.1016/j.jep.2010.02.002
PMID:20176100
Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Modified Si-Miao-San (mSMS) is a prescription modified from Si-Miao-San which is an ancient Chinese prescription used to treat various ailments.

AIM OF THE STUDY

Modified Si-Miao-San (mSMS) has been used for the treatment of infectious and inflammatory disorders in the clinic. This study was aimed to investigate its anti-inflammatory activity and underlying mechanism at cellular and molecular levels.

MATERIALS AND METHODS

We stimulated RAW264.7 cells with Lipopolysaccharide (LPS) and observed effects of mSMS on the release of inflammatory mediators such as: tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), NO, and relative gene expressions. Meanwhile, we also investigated the modulation of mSMS in inflammatory signal transduction mediated through extracellular signal-regulated protein kinase (ERK) and nuclear factor-kappaB (NF-kappaB) pathway.

RESULTS

Our findings demonstrated that mSMS significantly inhibited the excessive production of NO, TNF-alpha and IL-6 and the over expression of relative genes in LPS-stimulated macrophages. In addition, mSMS suppressed LPS-induced ERK1/2-phosphorylation and inhibited the activation of NF-kappaB by attenuation of I kappaB-alpha degradation.

CONCLUSIONS

Our results suggest that the anti-inflammatory properties of mSMS might result from the inhibition of inflammatory mediators, such as NO, TNF-alpha and IL-6, via suppression of ERK and NF-kappaB dependent pathways.

摘要

民族药理学相关性

改良四妙散(mSMS)是从四妙散(一种用于治疗各种疾病的古老中药方)改良而来的处方。

研究目的

改良四妙散(mSMS)已在临床上用于治疗感染和炎症性疾病。本研究旨在从细胞和分子水平上研究其抗炎活性及其潜在机制。

材料与方法

我们用脂多糖(LPS)刺激 RAW264.7 细胞,观察 mSMS 对炎症介质释放的影响,如肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、NO 和相对基因表达。同时,我们还研究了 mSMS 通过细胞外信号调节激酶(ERK)和核因子-κB(NF-κB)途径对炎症信号转导的调节作用。

结果

我们的研究结果表明,mSMS 能显著抑制 LPS 刺激的巨噬细胞中 NO、TNF-α和 IL-6 的过度产生和相对基因的过度表达。此外,mSMS 通过抑制 IκB-α降解,抑制 LPS 诱导的 ERK1/2 磷酸化,并抑制 NF-κB 的激活。

结论

我们的研究结果表明,mSMS 的抗炎作用可能是通过抑制炎症介质,如 NO、TNF-α和 IL-6,通过抑制 ERK 和 NF-κB 依赖的途径来实现的。

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