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螺旋藻提取物对脂多糖刺激的 RAW264.7 巨噬细胞的抗炎作用。

Anti-Inflammatory Effects of sp. Extract in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages.

机构信息

Department of Pharmacy, Sunchon National University, 255 Jungang-Ro, Suncheon 57922, Republic of Korea.

Department of Biology, Sunchon National University, 255 Jungang-Ro, Suncheon 57922, Republic of Korea.

出版信息

Biomed Res Int. 2022 Jul 14;2022:2717196. doi: 10.1155/2022/2717196. eCollection 2022.

DOI:10.1155/2022/2717196
PMID:35872858
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9303134/
Abstract

Lichens are a life form in which algae and fungi have a symbiotic relationship and have various biological activities, including anti-inflammatory and antiproliferative activities. This is the first study to investigate the anti-inflammatory activity of a sp. fungal extract (PSE) isolated from in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophage. PSE reduced the production of the proinflammatory cytokine (tumor necrosis factor-, interleukin-6, and interleukin-1), chemokine (granulocyte-macrophage colony-stimulating factor), nitric oxide, and prostaglandin E2 in the LPS-stimulated RAW264.7 macrophages. Especially, PSE inhibits the phosphorylation of activator protein-1 (AP-1) signaling (c-Fos and c-Jun) and their upstream mitogen-activated protein kinase kinases/mitogen-activated protein kinases (MKK/MAPKs: MKK4, MKK7, and JNK) and finally reduced the production of the inflammatory cytokines. The inhibitory effects mainly act via suppressing JNK-mediated AP-1 rather than the NF-B pathway. Furthermore, PSE inhibited the production of final inflammatory effector molecules involved in AP-1 signaling, including nitric oxide (NO) and prostaglandin E2 (PGE2). Here, we report that PSE has the potential to be developed as an anti-inflammatory agent.

摘要

地衣是一种藻类和真菌共生的生命形式,具有多种生物活性,包括抗炎和抗增殖活性。这是首次研究从 中分离得到的 真菌提取物(PSE)在脂多糖(LPS)刺激的 RAW 264.7 巨噬细胞中的抗炎活性。PSE 降低了 LPS 刺激的 RAW264.7 巨噬细胞中促炎细胞因子(肿瘤坏死因子-α、白细胞介素-6 和白细胞介素-1)、趋化因子(粒细胞-巨噬细胞集落刺激因子)、一氧化氮和前列腺素 E2 的产生。特别是,PSE 抑制了激活蛋白-1(AP-1)信号通路(c-Fos 和 c-Jun)及其上游丝裂原活化蛋白激酶激酶/丝裂原活化蛋白激酶(MKK/MAPKs:MKK4、MKK7 和 JNK)的磷酸化,最终减少了炎症细胞因子的产生。抑制作用主要通过抑制 JNK 介导的 AP-1 而不是 NF-κB 途径起作用。此外,PSE 抑制了参与 AP-1 信号通路的最终炎症效应分子的产生,包括一氧化氮(NO)和前列腺素 E2(PGE2)。在这里,我们报告 PSE 有可能被开发为一种抗炎剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/79da7a61876a/BMRI2022-2717196.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/4acc3f0398fa/BMRI2022-2717196.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/9db27cfb39a3/BMRI2022-2717196.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/79da7a61876a/BMRI2022-2717196.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/4acc3f0398fa/BMRI2022-2717196.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/0865cc3c571b/BMRI2022-2717196.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/7969ec6f26d6/BMRI2022-2717196.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/9db27cfb39a3/BMRI2022-2717196.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d0f/9303134/79da7a61876a/BMRI2022-2717196.007.jpg

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