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中华火星兰通过下调 NF-κB 信号通路和上调 HO-1/Nrf2 抗氧化蛋白抑制促炎介质的产生。

Spiranthes sinensis Suppresses Production of Pro-Inflammatory Mediators by Down-Regulating the NF-κB Signaling Pathway and Up-Regulating HO-1/Nrf2 Anti-Oxidant Protein.

机构信息

Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.

School of Pharmacy, China Medical University, Taichung, Taiwan.

出版信息

Am J Chin Med. 2015;43(5):969-89. doi: 10.1142/S0192415X15500561. Epub 2015 Jul 30.

DOI:10.1142/S0192415X15500561
PMID:26224027
Abstract

Spiranthes sinensis is an east Asian wild orchid used in Chinese folk medicine. In this study, an ethyl acetate fraction from S. sinensis(SSE) was found to suppress the production of LPS-stimulated inflammatory mediators in RAW264.7 cells and BALB/c mice. SSE inhibited the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), tumo necrosis factor-α (TNF-α), IL-1β, and IL-6 in LPS-stimulated RAW264.7 cells. SSE also significantly suppressed LPS-stimulated protein levels of iNOS and mPGES-1 by blocking IκB phosphorylation, NF-κB nuclear translocation, and MAPKs phosphorylation. In addition, SSE treatment also enhanced protein levels of HO-1 and anti-oxidant enzymes (SOD-1, CAT, and GPx-1) through the nuclear translocation of Nrf2 in LPS-stimulated RAW264.7 cells. In vivo, we demonstrated that SSE attenuated the levels of pro-inflammatory mediators (NO, TNF-α, IL-1β, and IL-6), ALT, and AST in the serum of LPS-stimulated BALB/c mice. Western blotting revealed that SSE enhanced HO-1 expression in lung and liver tissue after LPS injection in mice. These results suggest that the anti-inflammatory properties of SSE involve the suppression of iNOS, mPGES-1, and inflammatory mediators by inducing the HO-1 pathway in LPS-stimulated RAW264.7 cells and BALB/c mice.

摘要

春兰是一种东亚野生兰花,用于中国民间医学。在这项研究中,发现春兰的乙酸乙酯部分(SSE)可抑制 LPS 刺激的 RAW264.7 细胞和 BALB/c 小鼠中炎症介质的产生。SSE 抑制了 LPS 刺激的 RAW264.7 细胞中促炎介质如一氧化氮(NO)、前列腺素 E2(PGE2)、肿瘤坏死因子-α(TNF-α)、IL-1β和 IL-6 的产生。SSE 还通过阻断 IκB 磷酸化、NF-κB 核易位和 MAPKs 磷酸化,显著抑制 LPS 刺激的 iNOS 和 mPGES-1 蛋白水平。此外,SSE 处理还通过 LPS 刺激的 RAW264.7 细胞中 Nrf2 的核易位,增强 HO-1 和抗氧化酶(SOD-1、CAT 和 GPx-1)的蛋白水平。在体内,我们证明 SSE 减弱了 LPS 刺激的 BALB/c 小鼠血清中促炎介质(NO、TNF-α、IL-1β和 IL-6)、ALT 和 AST 的水平。Western blot 显示 SSE 增强了 LPS 注射后小鼠肺和肝组织中的 HO-1 表达。这些结果表明,SSE 的抗炎特性涉及通过诱导 LPS 刺激的 RAW264.7 细胞和 BALB/c 小鼠中的 HO-1 途径抑制 iNOS、mPGES-1 和炎症介质。

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