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金娃娃萱草通过抑制 NF-κB 和 MAPK 的激活抑制 LPS 刺激的人 PMA 分化 THP-1 细胞中 TLR4、NOD2、iNOS 和 COX-2 基因的表达。

Orostachys japonicus Inhibits Expression of the TLR4, NOD2, iNOS, and COX-2 Genes in LPS-Stimulated Human PMA-Differentiated THP-1 Cells by Inhibiting NF-κB and MAPK Activation.

机构信息

Department of Internal Medicine, College of Korean Medicine, Kyung Hee University, Seoul 130-872, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2015;2015:682019. doi: 10.1155/2015/682019. Epub 2015 Feb 24.

DOI:10.1155/2015/682019
PMID:25810745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4355124/
Abstract

Orostachys japonicus is traditionally used as an inflammatory agent. In this report, we investigated the effects of O. japonicus extract on the expression of genes encoding pathogen-recognition receptors (TLR2, TLR4, NOD1, and NOD2) and proinflammatory factors (iNOS, COX-2, and cytokines) in LPS-stimulated PMA-differentiated THP-1 cells and the NF-κB and MAPK pathways. O. japonicus induced toxicity at high concentrations but had no effect at concentrations lower than 25 μg/mL. O. japonicus inhibited LPS-induced TLR4 and NOD2 mRNA levels, suppressed LPS-induced iNOS and COX-2 transcription and translocation, and downregulated LPS-induced proinflammatory cytokine (IL-1β, IL-6, IL-8, and TNF-α) mRNA levels. In addition, O. japonicus inhibited LPS-induced NF-κB activation and IκBα degradation and suppressed LPS-induced JNK, p38 MAPK, and ERK phosphorylation. Overall, our results demonstrate that the anti-inflammatory effects of O. japonicus are mediated by suppression of NF-κB and MAPK signaling, resulting in reduced TLR4, NOD2, iNOS, and COX-2 expression and inhibition of inflammatory cytokine expression.

摘要

瓦松被传统用作一种炎症介质。在本报告中,我们研究了瓦松提取物对 LPS 刺激的 PMA 分化 THP-1 细胞中编码病原体识别受体(TLR2、TLR4、NOD1 和 NOD2)和促炎因子(iNOS、COX-2 和细胞因子)的基因表达以及 NF-κB 和 MAPK 通路的影响。瓦松在高浓度下具有细胞毒性,但在低于 25μg/mL 的浓度下没有影响。瓦松抑制 LPS 诱导的 TLR4 和 NOD2 mRNA 水平,抑制 LPS 诱导的 iNOS 和 COX-2 转录和易位,并下调 LPS 诱导的促炎细胞因子(IL-1β、IL-6、IL-8 和 TNF-α)mRNA 水平。此外,瓦松抑制 LPS 诱导的 NF-κB 激活和 IκBα 降解,并抑制 LPS 诱导的 JNK、p38 MAPK 和 ERK 磷酸化。总的来说,我们的结果表明,瓦松的抗炎作用是通过抑制 NF-κB 和 MAPK 信号转导介导的,从而减少 TLR4、NOD2、iNOS 和 COX-2 的表达,并抑制炎症细胞因子的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/15ee92c6ae20/ECAM2015-682019.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/03f9c22d4e46/ECAM2015-682019.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/2ba95d65aba7/ECAM2015-682019.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/b3d291ff533f/ECAM2015-682019.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/5dfb13da77bc/ECAM2015-682019.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/60d69a38889a/ECAM2015-682019.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/15ee92c6ae20/ECAM2015-682019.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/03f9c22d4e46/ECAM2015-682019.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/2ba95d65aba7/ECAM2015-682019.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/b3d291ff533f/ECAM2015-682019.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/5dfb13da77bc/ECAM2015-682019.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/60d69a38889a/ECAM2015-682019.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3fe3/4355124/15ee92c6ae20/ECAM2015-682019.006.jpg

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