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KIOM-MA 一种新型草药在 LPS 刺激的 RAW 264.7 巨噬细胞中发挥抗炎作用。

A Novel Herbal Medicine KIOM-MA Exerts an Anti-Inflammatory Effect in LPS-Stimulated RAW 264.7 Macrophage Cells.

机构信息

Korean Medicine (KM)-Based Herbal Drug Research Group, Korea Institute of Oriental Medicine, 461-24 Jeonmin-Dong, Yuseong, Daejeon 305-811, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2012;2012:462383. doi: 10.1155/2012/462383. Epub 2012 Nov 27.

DOI:10.1155/2012/462383
PMID:23243447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3518860/
Abstract

KIOM-MA was recently reported as a novel herbal medicine effective for atopic dermatitis and asthma. In this study, we have demonstrated the inhibitory effect of KIOM-MA on proinflammatory mediator produced in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. KIOM-MA significantly inhibited the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as nitric oxide (NO) and prostaglandin E(2) (PGE(2)). Consistent with the inhibitory effect on PGE(2), KIOM-MA suppresses the LPS-induced migration of macrophages and gelatinase activity and the expression of matrix metalloprotease-9 (MMP-9) in a dose-dependent manner. Additionally, KIOM-MA showed a strong suppressive effect on the inflammatory cytokines production such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). We also found that KIOM-MA inhibits the activation of nuclear factor-κB (NF-κB) and represses the activity of extracellular signal-regulated kinase (ERK), p38, and c-Jun NH(2)-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs). Taken together, we elucidated the mechanism of anti-inflammatory effect of KIOM-MA using RAW 264.7 cells stimulated by LPS.

摘要

KIOM-MA 最近被报道为一种治疗特应性皮炎和哮喘的新型草药。在这项研究中，我们已经证明了 KIOM-MA 对脂多糖 (LPS) 刺激的 RAW 264.7 细胞中促炎介质的抑制作用。KIOM-MA 显著抑制诱导型一氧化氮合酶 (iNOS) 和环氧化酶-2 (COX-2) 的表达以及一氧化氮 (NO) 和前列腺素 E(2) (PGE(2))。与对 PGE(2) 的抑制作用一致，KIOM-MA 以剂量依赖性方式抑制巨噬细胞和明胶酶活性以及基质金属蛋白酶-9 (MMP-9) 的 LPS 诱导迁移。此外，KIOM-MA 对肿瘤坏死因子-α (TNF-α) 和白细胞介素-6 (IL-6) 等炎症细胞因子的产生表现出强烈的抑制作用。我们还发现 KIOM-MA 抑制核因子-κB (NF-κB) 的激活，并抑制细胞外信号调节激酶 (ERK)、p38 和 c-Jun NH(2)-末端激酶 (JNK) 丝裂原激活蛋白激酶 (MAPKs) 的活性。综上所述，我们使用 LPS 刺激的 RAW 264.7 细胞阐明了 KIOM-MA 的抗炎作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/32e51c3d106a/ECAM2012-462383.009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/32e51c3d106a/ECAM2012-462383.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/2c93ef718f0f/ECAM2012-462383.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/a192d7f6d710/ECAM2012-462383.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/56bf91e1f27c/ECAM2012-462383.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/cf2ca1ebf831/ECAM2012-462383.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/a4a65d6636a8/ECAM2012-462383.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7cc7/3518860/cedac63ec92f/ECAM2012-462383.008.jpg
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