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茵陈的花能减轻炎症反应。

Flowers of Inula japonica Attenuate Inflammatory Responses.

机构信息

Research and Development Division, Daegu Gyeongbuk Institute for Oriental Medicine Industry, Gyeongsan 712-210, Korea.

出版信息

Immune Netw. 2010 Oct;10(5):145-52. doi: 10.4110/in.2010.10.5.145. Epub 2010 Oct 31.

DOI:10.4110/in.2010.10.5.145
PMID:21165243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2993946/
Abstract

BACKGROUND

The flowers of Inula japonica (Inulae Flos) have long been used in traditional medicine for the treatment of inflammatory diseases. In the present study, we investigated the anti-inflammatory properties of Inulae Flos Extract (IFE).

METHODS

The anti-inflammatory effects of IFE against nitric oxide (NO), PGE(2), TNF-α, and IL-6 release, as well as NF-κB and MAP kinase activation were evaluated in RAW 264.7 cells.

RESULTS

IFE inhibited the production of NO and the expression of inducible nitric oxide synthase (iNOS) in LPS-stimulated RAW264.7 cells. In addition, IFE reduced the release of pro-inflammatory cytokines, such as TNF-α and IL-6. Furthermore, IFE inhibited the NF-κB activation induced by LPS, which was associated with the abrogation of IκB-α degradation and subsequent decreases in nuclear p65 and p50 levels. Moreover, the phosphorylation of ERK, JNK, and p38 MAP kinases in LPS-stimulated RAW 264.7 cells was suppressed by IFE in a dose-dependent manner.

CONCLUSION

These results suggest that the anti-inflammation activities of IFE might be attributed to the inhibition of NO, iNOS and cytokine expression through the down-regulation of NF-κB activation via suppression of IκBα and MAP kinase phosphorylation in macrophages.

摘要

背景

旋覆花（Inulae Flos）的花朵在传统医学中一直被用于治疗炎症性疾病。在本研究中，我们研究了旋覆花提取物（IFE）的抗炎特性。

方法

在 RAW 264.7 细胞中，评估了 IFE 对一氧化氮（NO）、PGE（2）、TNF-α 和 IL-6 释放以及 NF-κB 和 MAP 激酶激活的抗炎作用。

结果

IFE 抑制了 LPS 刺激的 RAW264.7 细胞中 NO 的产生和诱导型一氧化氮合酶（iNOS）的表达。此外，IFE 减少了促炎细胞因子如 TNF-α和 IL-6 的释放。此外，IFE 抑制了 LPS 诱导的 NF-κB 激活，这与 IκB-α降解的阻断以及随后核 p65 和 p50 水平的降低有关。此外，IFE 以剂量依赖的方式抑制了 LPS 刺激的 RAW 264.7 细胞中 ERK、JNK 和 p38 MAP 激酶的磷酸化。

结论

这些结果表明，IFE 的抗炎活性可能归因于通过抑制 IκBα 和 MAP 激酶磷酸化来抑制 NF-κB 激活，从而抑制 NO、iNOS 和细胞因子表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/5cb294bf9bd1/in-10-145-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/8352e7265bae/in-10-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/daaf4eaa45fb/in-10-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/7c57f3ae8d95/in-10-145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/344d95a1788c/in-10-145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/5cb294bf9bd1/in-10-145-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/8352e7265bae/in-10-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/daaf4eaa45fb/in-10-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/7c57f3ae8d95/in-10-145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/344d95a1788c/in-10-145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fd6/2993946/5cb294bf9bd1/in-10-145-g005.jpg

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