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姜黄素和四氢姜黄素对葡聚糖硫酸钠诱导的小鼠结肠炎及炎症信号的比较作用

Comparative Effects of Curcumin and Tetrahydrocurcumin on Dextran Sulfate Sodium-induced Colitis and Inflammatory Signaling in Mice.

作者信息

Yang Joon-Yeop, Zhong Xiancai, Kim Su-Jung, Kim Do-Hee, Kim Hyun Soo, Lee Jeong-Sang, Yum Hye-Won, Lee Jeewoo, Na Hye-Kyung, Surh Young-Joon

机构信息

Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul, Korea.

Department of Functional Food and Biotechnology, College of Medical Science, Jeonju University, Jeonju, Korea.

出版信息

J Cancer Prev. 2018 Mar;23(1):18-24. doi: 10.15430/JCP.2018.23.1.18. Epub 2018 Mar 30.

DOI:10.15430/JCP.2018.23.1.18
PMID:29629345
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5886491/
Abstract

BACKGROUND

Curcumin, a yellow ingredient of turmeric ( Linn, Zingiberaceae), has long been used in traditional folk medicine in the management of inflammatory disorders. Although curcumin has been reported to inhibit experimentally-induced colitis and carcinogenesis, the underlying molecular mechanisms remain largely unresolved.

METHODS

Murine colitis was induced by dextran sulfate sodium (DSS) which mimics inflammatory bowel disease. Curcumin or tetrahydrocurcumin was given orally (0.1 or 0.25 mmol/kg body weight daily) for 7 days before and together with DSS administration (3% in tap water). Collected colon tissue was used for histologic and biochemical analyses.

RESULTS

Administration of curcumin significantly attenuated the severity of DSS-induced colitis and the activation of NF-κB and STAT3 as well as expression of COX-2 and inducible nitric oxide synthase. In contrast to curcumin, its non-electrophilic analogue, tetrahydrocurcumin has much weaker inhibitory effects.

CONCLUSIONS

Intragastric administration of curcumin inhibited the experimentally induced murine colitis, which was associated with inhibition of pro-inflammatory signaling mediated by NF-κB and STAT3.

摘要

背景

姜黄素是姜黄(姜科,姜黄属)的黄色成分,长期以来一直用于传统民间医学中治疗炎症性疾病。尽管有报道称姜黄素可抑制实验性诱导的结肠炎和致癌作用,但其潜在的分子机制仍 largely 未得到解决。

方法

用模拟炎症性肠病的葡聚糖硫酸钠(DSS)诱导小鼠结肠炎。在给予 DSS(自来水中 3%)之前和同时,口服给予姜黄素或四氢姜黄素(每日 0.1 或 0.25 mmol/kg 体重),持续 7 天。收集结肠组织用于组织学和生化分析。

结果

给予姜黄素可显著减轻 DSS 诱导的结肠炎的严重程度,以及 NF-κB 和 STAT3 的激活以及 COX-2 和诱导型一氧化氮合酶的表达。与姜黄素相比,其非亲电类似物四氢姜黄素的抑制作用要弱得多。

结论

胃内给予姜黄素可抑制实验性诱导的小鼠结肠炎,这与抑制由 NF-κB 和 STAT3 介导的促炎信号有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/a3ad78dd32a3/jcp-23-018f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/4fc5938c11e0/jcp-23-018f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/d6ed8dbf6cbc/jcp-23-018f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/f7d05199f850/jcp-23-018f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/7620c11e97fc/jcp-23-018f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/a3ad78dd32a3/jcp-23-018f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/4fc5938c11e0/jcp-23-018f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/d6ed8dbf6cbc/jcp-23-018f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/f7d05199f850/jcp-23-018f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/7620c11e97fc/jcp-23-018f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8229/5886491/a3ad78dd32a3/jcp-23-018f5.jpg

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