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甘菊、薄荷、格拉伯草本混合物对脂多糖刺激的 RAW264.7 巨噬细胞的抗炎作用。

Anti‑inflammatory effect of , peppermint, glabra herbal mixture in lipopolysaccharide‑stimulated RAW264.7 macrophages.

机构信息

Department of Food Science, Institute of Health Science, Jeonju University, Jeonju‑si, Jeollabuk‑do 55069, Republic of Korea.

Department of Food Science and Technology, Jeonbuk National University, Jeonju‑si, Jeollabuk‑do 54896, Republic of Korea.

出版信息

Mol Med Rep. 2021 Jul;24(1). doi: 10.3892/mmr.2021.12171. Epub 2021 May 26.

DOI:10.3892/mmr.2021.12171
PMID:34036392
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8170225/
Abstract

The normal inflammatory reaction protects the body from harmful external factors, whereas abnormal chronic inflammation can cause various diseases, including cancer. The purpose of the present study was to investigate the anti‑inflammatory activity of a mixture of , peppermint and (CPG) by analyzing the expression levels of inflammatory mediators, cytokines and transcription factors in lipopolysaccharide (LPS)‑stimulated Raw264.7 cells. A nitric oxide assay, ELISA, western blotting and immunofluorescence staining were performed to investigate the anti‑inflammatory activity of the CPG mixture. Pretreatment of Raw264.7 cells with CPG inhibited the increase of inflammatory mediators (inducible nitric oxide synthase, cyclooxygenase‑2 and IFN‑β) induced by LPS. Additionally, it inhibited the production of pro‑inflammatory cytokines (TNF‑α, IL‑6 and IL‑1β). CPG suppressed LPS‑induced phosphorylation of STAT1, AKT, Iκb and NF‑κB. Furthermore, CPG inhibited the translocation of NF‑κB into the nucleus. In summary, CPG could inhibit LPS‑induced inflammation, which occurs primarily through the AKT/Iκb/NF‑κB signaling pathway in RAW264.7 cells.

摘要

正常的炎症反应可保护机体免受有害的外部因素的侵害,而异常的慢性炎症可导致各种疾病,包括癌症。本研究旨在通过分析脂多糖 (LPS) 刺激的 Raw264.7 细胞中炎症介质、细胞因子和转录因子的表达水平,研究薄荷、留兰香和迷迭香(CPG)混合物的抗炎活性。通过一氧化氮测定法、ELISA、western blot 和免疫荧光染色来研究 CPG 混合物的抗炎活性。CPG 预处理 Raw264.7 细胞可抑制 LPS 诱导的炎症介质(诱导型一氧化氮合酶、环氧化酶-2 和 IFN-β)的增加。此外,它还抑制了促炎细胞因子(TNF-α、IL-6 和 IL-1β)的产生。CPG 抑制 LPS 诱导的 STAT1、AKT、Iκb 和 NF-κB 的磷酸化。此外,CPG 抑制 NF-κB 向核内易位。综上所述,CPG 可抑制 LPS 诱导的炎症,其主要通过 RAW264.7 细胞中的 AKT/Iκb/NF-κB 信号通路发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/4a6b39e8ae7f/mmr-24-01-12171-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/e7fe357ea0a4/mmr-24-01-12171-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/33261084d8b8/mmr-24-01-12171-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/4a6b39e8ae7f/mmr-24-01-12171-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/e7fe357ea0a4/mmr-24-01-12171-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/392fcc0700eb/mmr-24-01-12171-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/ba5fd5df39c7/mmr-24-01-12171-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/33261084d8b8/mmr-24-01-12171-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/013d/8170225/4a6b39e8ae7f/mmr-24-01-12171-g04.jpg

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