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发酵物的氯仿提取物通过抑制诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）调节脂多糖（LPS）诱导的RAW 264.7细胞炎症反应。

Chloroform Extract from Fermented Regulates LPS-Induced Inflammation Response in RAW 264.7 Cells by Inhibiting iNOS and COX-2.

作者信息

Kim Hyunju, Kim Kyoung-Sook, Lee Young-Choon, Cho Jong Hyun

机构信息

Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan 49315, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2024 Dec 12;35:e2408047. doi: 10.4014/jmb.2408.08047.

DOI:10.4014/jmb.2408.08047
PMID:39849923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11813387/
Abstract

Inflammatory is a crucial part of the immune system of body protect it from harmful invaders, such as bacteria, viruses, and other foreign substances. In this study, the effects of chloroform extract of fermented (CEFV) on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 macrophages were investigated. The CEFV significantly inhibited NO production and reduced the expression of inducible nitric oxide synthase (iNOS) at both protein and mRNA levels in a dose-dependent manner. Also, CEFV decreased PGE2 production, suppressed COX-2 expression, and inhibited the activation of the ERK and JNK pathways but not the p38 pathway. Taken together, CEFV suppressed NF-κB activation, which is a key regulator in the inflammatory response. The main phenolic compounds identified in CEFV were tectoridin, luteolin, resveratrol, and hesperetin. Therefore, in this study, CEFC exhibits potent anti-inflammatory effects by downregulating the production of pro-inflammatory mediators and inhibiting key inflammatory pathway in RAW264.7 cells.

摘要

炎症是身体免疫系统的关键部分，可保护身体免受有害入侵者的侵害，如细菌、病毒和其他外来物质。在本研究中，研究了发酵物氯仿提取物（CEFV）对脂多糖（LPS）诱导的RAW264.7巨噬细胞炎症反应的影响。CEFV以剂量依赖性方式显著抑制NO生成，并在蛋白质和mRNA水平上降低诱导型一氧化氮合酶（iNOS）的表达。此外，CEFV减少PGE2生成，抑制COX-2表达，并抑制ERK和JNK通路的激活，但不影响p38通路。综上所述，CEFV抑制了NF-κB的激活，而NF-κB是炎症反应中的关键调节因子。在CEFV中鉴定出的主要酚类化合物为鸢尾苷、木犀草素、白藜芦醇和橙皮素。因此，在本研究中，CEFC通过下调促炎介质的产生并抑制RAW264.7细胞中的关键炎症通路而表现出强大的抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/41521e297c21/jmb-35-e2408047-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/84f3261399f4/jmb-35-e2408047-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/af3ab06e0b80/jmb-35-e2408047-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/a4a64c02da53/jmb-35-e2408047-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/083fcf8303b4/jmb-35-e2408047-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/33786e961679/jmb-35-e2408047-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/41521e297c21/jmb-35-e2408047-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/84f3261399f4/jmb-35-e2408047-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/af3ab06e0b80/jmb-35-e2408047-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/a4a64c02da53/jmb-35-e2408047-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/083fcf8303b4/jmb-35-e2408047-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/33786e961679/jmb-35-e2408047-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80b0/11813387/41521e297c21/jmb-35-e2408047-f6.jpg

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本文引用的文献

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Tectoridin alleviates lipopolysaccharide-induced inflammation inhibiting TLR4-NF-κB/NLRP3 signaling and .朝藿定 C 减轻脂多糖诱导的炎症，抑制 TLR4-NF-κB/NLRP3 信号通路。
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