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MCL通过抑制NF-κB和NLRP3炎性小体激活在诱导的免疫反应中发挥抗炎作用。

MCL Plays an Anti-Inflammatory Role in -Induced Immune Response by Inhibiting NF-B and NLRP3 Inflammasome Activation.

作者信息

Zhang Qingwen, Jiang Xinru, He Weigang, Wei Kailin, Sun Jinxia, Qin Xiangyang, Zheng Yuejuan, Jiang Xin

机构信息

Department of Immunology and Microbiology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.

Major in Biology, The University of British Columbia, Vancouver, Canada V6T 1Z4.

出版信息

Mediators Inflamm. 2017;2017:2432904. doi: 10.1155/2017/2432904. Epub 2017 May 31.

DOI:10.1155/2017/2432904
PMID:28642632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5470027/
Abstract

(Mtb) remains a significant menace to global health as it induces granulomatous lung lesions and systemic inflammatory responses during active tuberculosis (TB). Micheliolide (MCL), a sesquiterpene lactone, was recently reported to have a function of relieving LPS-induced inflammatory response, but the regulative role of MCL on the immunopathology of TB still remains unknown. In this experiment, we examined the inhibitory effect of MCL on Mtb-induced inflammatory response in mouse macrophage-like cell line Raw264.7 by downregulating the activation of nuclear factor kappa B (NF-B) and NLRP3 inflammasome. Evidences showed that MCL decreased the secretion of Mtb-induced inflammatory cytokines (IL-1 and TNF-) in a dose-dependent manner. Meanwhile, MCL dramatically suppressed Mtb-induced activation of iNOS and COX2 as well as subsequent production of NO. Furthermore, MCL inhibited Mtb-induced phosphorylation of Akt (Ser 473) in Raw264.7. According to our results, MCL plays an important role in modulating Mtb-induced inflammatory response through PI3K/Akt/NF-B pathway and subsequently downregulating the activation of NLRP3 inflammasome. Therefore, MCL may represent as a potential drug candidate in the adjuvant treatment of TB by regulating host immune response.

摘要

结核分枝杆菌（Mtb）仍是全球健康的重大威胁，因为在活动性肺结核（TB）期间，它会引发肺部肉芽肿病变和全身炎症反应。米氏内酯（MCL）是一种倍半萜内酯，最近有报道称其具有减轻脂多糖诱导的炎症反应的功能，但MCL对结核病免疫病理学的调节作用仍不清楚。在本实验中，我们通过下调核因子κB（NF-κB）和NLRP3炎性小体的激活，研究了MCL对小鼠巨噬细胞样细胞系Raw264.7中Mtb诱导的炎症反应的抑制作用。证据表明，MCL以剂量依赖性方式降低了Mtb诱导的炎症细胞因子（IL-1和TNF-）的分泌。同时，MCL显著抑制了Mtb诱导的iNOS和COX2的激活以及随后NO的产生。此外，MCL抑制了Mtb诱导的Raw264.7中Akt（Ser 473）的磷酸化。根据我们的结果，MCL通过PI3K/Akt/NF-κB途径在调节Mtb诱导的炎症反应中发挥重要作用，随后下调NLRP3炎性小体的激活。因此，MCL可能通过调节宿主免疫反应成为结核病辅助治疗的潜在候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/b7dac98b744e/MI2017-2432904.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/cadd24adf2f7/MI2017-2432904.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/c8800a53e0f8/MI2017-2432904.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/97c7e3034417/MI2017-2432904.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/c0a2bb33ff53/MI2017-2432904.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/237c9242a365/MI2017-2432904.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/404302f27949/MI2017-2432904.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/f3088f29e53a/MI2017-2432904.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/b7dac98b744e/MI2017-2432904.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/cadd24adf2f7/MI2017-2432904.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/c8800a53e0f8/MI2017-2432904.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/97c7e3034417/MI2017-2432904.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/c0a2bb33ff53/MI2017-2432904.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/237c9242a365/MI2017-2432904.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/404302f27949/MI2017-2432904.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/f3088f29e53a/MI2017-2432904.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1642/5470027/b7dac98b744e/MI2017-2432904.008.jpg

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