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黄花蒿乙酸乙酯提取物具有显著的抗炎作用。

Ethyl Acetate Extract of Artemisia anomala S. Moore Displays Potent Anti-Inflammatory Effect.

机构信息

Shanghai University of Traditional Chinese Medicine, Pudong, Shanghai 201203, China.

出版信息

Evid Based Complement Alternat Med. 2014;2014:681352. doi: 10.1155/2014/681352. Epub 2014 Mar 12.

DOI:10.1155/2014/681352
PMID:24744815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3972921/
Abstract

Artemisia anomala S. Moore has been widely used in China to treat inflammatory diseases for hundreds of years. However, mechanisms associated with its anti-inflammatory effect are not clear. In this study, we prepared ethyl acetate, petroleum ether, n-BuOH, and aqueous extracts from ethanol extract of Artemisia anomala S. Moore. Comparing anti-inflammatory effects of these extracts, we found that ethyl acetate extract of this herb (EAFA) exhibited the strongest inhibitory effect on nitric oxide (NO) production in LPS/IFN γ -stimulated RAW264.7 cells. EAFA suppressed the production of NO in a time- and dose-dependent manner without eliciting cytotoxicity to RAW264.7 cells. To understand the molecular mechanism underlying EAFA's anti-inflammatory effect, we showed that EAFA increased total cellular anti-oxidant capacity while reducing the amount of inducible nitric oxide synthase (iNOS) in stimulated RAW264.7 cells. EAFA also suppressed the expression of IL-1 β and IL-6, whereas it elevates the level of heme oxygenase-1. These EAFA-induced events were apparently associated with NF- κ B and MAPK signaling pathways because the DNA binding activity of p50/p65 was impaired and the activities of both ERK and JNK were decreased in EFEA-treated cells comparing to untreated cells. Our findings suggest that EAFA exerts its anti-inflammatory effect by inhibiting the expression of iNOS.

摘要

青蒿已在中国被广泛用于治疗炎症性疾病数百年。然而,其抗炎作用的机制尚不清楚。在本研究中,我们从青蒿乙醇提取物中制备了乙酸乙酯、石油醚、正丁醇和水提取物。比较这些提取物的抗炎效果,我们发现该草药的乙酸乙酯提取物(EAFA)对 LPS/IFNγ刺激的 RAW264.7 细胞中一氧化氮(NO)的产生具有最强的抑制作用。EAFA 以时间和剂量依赖的方式抑制 NO 的产生,而对 RAW264.7 细胞没有细胞毒性。为了了解 EAFA 抗炎作用的分子机制,我们表明 EAFA 增加了细胞总抗氧化能力,同时减少了刺激的 RAW264.7 细胞中诱导型一氧化氮合酶(iNOS)的数量。EAFA 还抑制了 IL-1β和 IL-6 的表达,同时提高了血红素加氧酶-1 的水平。这些 EAFA 诱导的事件显然与 NF-κB 和 MAPK 信号通路有关,因为与未处理的细胞相比,p50/p65 的 DNA 结合活性受损,并且 ERK 和 JNK 的活性降低。我们的研究结果表明,EAFA 通过抑制 iNOS 的表达发挥其抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c720578b6797/ECAM2014-681352.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/ce99e75b1c3c/ECAM2014-681352.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/24fb734a41bf/ECAM2014-681352.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/8bca9bbd908f/ECAM2014-681352.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c993f39b4a04/ECAM2014-681352.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c10fe1bd62c2/ECAM2014-681352.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c720578b6797/ECAM2014-681352.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/ce99e75b1c3c/ECAM2014-681352.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/24fb734a41bf/ECAM2014-681352.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/8bca9bbd908f/ECAM2014-681352.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c993f39b4a04/ECAM2014-681352.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c10fe1bd62c2/ECAM2014-681352.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8487/3972921/c720578b6797/ECAM2014-681352.006.jpg

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