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白藜芦醇通过抑制 TLR4/NF-κBp65/MAPKs 信号通路减轻脂多糖介导的大鼠急性炎症。

Resveratrol mitigates lipopolysaccharide-mediated acute inflammation in rats by inhibiting the TLR4/NF-κBp65/MAPKs signaling cascade.

机构信息

Natural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, China.

Key laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China.

出版信息

Sci Rep. 2017 Mar 21;7:45006. doi: 10.1038/srep45006.

DOI:10.1038/srep45006
PMID:28322346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5359552/
Abstract

Resveratrol (RSV) is a natural compound exhibiting anti-inflammatory effect, but the anti-inflammatory mechanism has not been fully understood. This study is aimed to evaluate the anti-inflammatory activity and mechanism of RSV in lipopolysaccharides-induced rats' model. The visceral wet/dry weight ratios and the changes of hematologic and biochemical indices indicated that LPS- stimulation mainly caused damages to liver and lung, while pretreatment with RSV could alleviate the lesions. The cytokine assays showed that RSV could markedly decrease the production of proinflammatory mediators and cytokines (IL-1, IL-1β, IL-6, NO, iNOS and COX-2), and increase the expression of anti-inflammatory mediator (IL-10). RSV could inhibit TLR4 signaling pathway by down-regulating the mRNA levels of MyD88 and TRAF6, and suppressing the TLR4 protein. RSV could inhibit the signaling cascades of NF-κBp65 and MAPKs through down-regulating the mRNA levels of IκBα, p38MAPK, JNK, ERK1, ERK2 and ERK5 in liver and lung, and suppressing the dynamic changes of proteins and phosphorylated proteins including IκBα, NF-κBp65, p38MAPK, JNK, ERK1/2 and ERK5 from tissue's cytoplasm to nucleus. In conclusion, RSV possessed a therapeutic effect on LPS-induced inflammation in rats and the mechanism mainly attributed to suppressing the signaling cascades of NF-κBp65 and MAPKs by inhibiting the TLR4 signaling pathway.

摘要

白藜芦醇（RSV）是一种具有抗炎作用的天然化合物，但抗炎机制尚未完全阐明。本研究旨在评估 RSV 在脂多糖诱导的大鼠模型中的抗炎活性和机制。内脏湿/干重比和血液学及生化指标的变化表明，LPS 刺激主要导致肝脏和肺部损伤，而 RSV 预处理可减轻损伤。细胞因子检测表明，RSV 可显著降低促炎介质和细胞因子（IL-1、IL-1β、IL-6、NO、iNOS 和 COX-2）的产生，并增加抗炎介质（IL-10）的表达。RSV 可通过下调 TLR4 信号通路中的 MyD88 和 TRAF6 mRNA 水平，并抑制 TLR4 蛋白，抑制 TLR4 信号通路。RSV 可通过下调肝脏和肺部中 IκBα、p38MAPK、JNK、ERK1、ERK2 和 ERK5 的 mRNA 水平，抑制 IκBα、NF-κBp65、p38MAPK、JNK、ERK1/2 和 ERK5 等蛋白及其磷酸化蛋白从组织细胞质向细胞核的动态变化，抑制 NF-κBp65 和 MAPKs 的信号级联反应。综上所述，RSV 对 LPS 诱导的大鼠炎症具有治疗作用，其机制主要归因于通过抑制 TLR4 信号通路抑制 NF-κBp65 和 MAPKs 的信号级联反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/7b87dfbd381a/srep45006-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/67667fd438ca/srep45006-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/4936b33ee99f/srep45006-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/20de188f4e05/srep45006-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/675c088f37a1/srep45006-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/b3019900b621/srep45006-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/7b87dfbd381a/srep45006-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/67667fd438ca/srep45006-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/4936b33ee99f/srep45006-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/20de188f4e05/srep45006-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/675c088f37a1/srep45006-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/b3019900b621/srep45006-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e2c/5359552/7b87dfbd381a/srep45006-f6.jpg

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