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姜黄素可消除 LPS 诱导的 RAW 264.7 巨噬细胞中促炎细胞因子。涉及 SOCS-1、-3 和 p38MAPK 的新机制证据。

Curcumin abrogates LPS-induced pro-inflammatory cytokines in RAW 264.7 macrophages. Evidence for novel mechanisms involving SOCS-1, -3 and p38 MAPK.

机构信息

Department of Diagnosis and Surgery, Faculdade de Odontologia de Araraquara, Univ Estadual Paulista (UNESP), Araraquara, SP, Brazil.

出版信息

Arch Oral Biol. 2013 Oct;58(10):1309-17. doi: 10.1016/j.archoralbio.2013.07.005. Epub 2013 Aug 23.

DOI:10.1016/j.archoralbio.2013.07.005
PMID:24011306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4030384/
Abstract

Curcumin is the active compound in the extract of Curcuma longa rhizomes with anti-inflammatory properties mediated by inhibition of intracellular signalling. SOCS and MAPKinases are involved in the signalling events controlling the expression of IL-6, TNF-α and PGE2, which have important roles on chronic inflammatory diseases. The aim was to assess if these pathways are involved in curcumin-mediated effects on LPS-induced expression of these cytokines in macrophages. RAW 264.7 murine macrophages were stimulated with Escherichia coli LPS in the presence and absence of non-cytotoxic concentrations of curcumin. Curcumin potently inhibited LPS-induced expression of IL-6, TNF-α and COX-2 mRNA and prevented LPS-induced inhibition of SOCS-1 and -3 expression and the inhibition of the activation of p38 MAPKinase by modulation of its nuclear translocation. In conclusion, curcumin potently inhibits expression of LPS-induced inflammatory cytokines in macrophages via mechanisms that involve modulation of expression and activity of SOCS-1 and SOCS-3 and of p38 MAPK.

摘要

姜黄素是姜黄根茎提取物中的活性化合物,具有抗炎特性,其作用机制是抑制细胞内信号转导。SOCS 和 MAPK 激酶参与控制 IL-6、TNF-α 和 PGE2 表达的信号事件,这些细胞因子在慢性炎症性疾病中具有重要作用。本研究旨在评估这些途径是否参与姜黄素介导的对 LPS 诱导的巨噬细胞细胞因子表达的影响。用大肠杆菌 LPS 刺激 RAW 264.7 鼠巨噬细胞,同时存在和不存在非细胞毒性浓度的姜黄素。姜黄素强烈抑制 LPS 诱导的 IL-6、TNF-α 和 COX-2 mRNA 的表达,并通过调节其核易位来防止 LPS 诱导的 SOCS-1 和 SOCS-3 表达抑制以及 p38 MAPK 激活的抑制。总之,姜黄素通过调节 SOCS-1 和 SOCS-3 以及 p38 MAPK 的表达和活性,强烈抑制巨噬细胞中 LPS 诱导的炎症细胞因子的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/03434e359375/nihms-510867-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/17300e1dbe22/nihms-510867-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/81cb83a658f6/nihms-510867-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/5b31033ce856/nihms-510867-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/801d9537d814/nihms-510867-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/cfdd41e2cfd0/nihms-510867-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/03434e359375/nihms-510867-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/17300e1dbe22/nihms-510867-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/81cb83a658f6/nihms-510867-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/5b31033ce856/nihms-510867-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/801d9537d814/nihms-510867-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/cfdd41e2cfd0/nihms-510867-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28f3/4030384/03434e359375/nihms-510867-f0006.jpg

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