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当归乙醇提取物通过抑制环氧化酶-前列腺素途径抑制巴豆油诱导的炎症。

Ethanol extract of Angelica gigas inhibits croton oil-induced inflammation by suppressing the cyclooxygenase - prostaglandin pathway.

作者信息

Shin Sunhee, Joo Seong Soo, Park Dongsun, Jeon Jeong Hee, Kim Tae Kyun, Kim Jeong Seon, Park Sung Kyeong, Hwang Bang Yeon, Kim Yun-Bae

机构信息

College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju, Korea.

出版信息

J Vet Sci. 2010 Mar;11(1):43-50. doi: 10.4142/jvs.2010.11.1.43.

DOI:10.4142/jvs.2010.11.1.43
PMID:20195064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2833429/
Abstract

The anti-inflammatory effects of an ethanol extract of Angelica gigas (EAG) were investigated in vitro and in vivo using croton oil-induced inflammation models. Croton oil (20 microg/mL) up-regulated mRNA expression of cyclooxygenase (COX)-I and COX-II in the macrophage cell line, RAW 264.7, resulting in the release of high concentrations of prostaglandin E(2) (PGE(2)). EAG (1 approximately 10 microg/mL) markedly suppressed croton oil-induced COX-II mRNA expression and PGE(2) production. Application of croton oil (5% in acetone) to mouse ears caused severe local erythema, edema and vascular leakage, which were significantly attenuated by oral pre-treatment with EAG (50 approximately 500 mg/kg). Croton oil dramatically increased blood levels of interleukin (IL)-6 and PGE(2) without affecting tumor-necrosis factor (TNF)-alpha and nitric oxide (NO) levels. EAG pre-treatment remarkably lowered IL-6 and PGE(2), but did not alter TNF-alpha or NO concentrations. These results indicate that EAG attenuates inflammatory responses in part by blocking the COX - PGE(2) pathway. Therefore, EAG could be a promising candidate for the treatment of inflammatory diseases.

摘要

利用巴豆油诱导的炎症模型，在体外和体内研究了当归乙醇提取物（EAG）的抗炎作用。巴豆油（20微克/毫升）上调巨噬细胞系RAW 264.7中环氧合酶（COX）-I和COX-II的mRNA表达，导致高浓度前列腺素E2（PGE2）的释放。EAG（1至10微克/毫升）显著抑制巴豆油诱导的COX-II mRNA表达和PGE2产生。将巴豆油（5%丙酮溶液）涂抹于小鼠耳部可引起严重的局部红斑、水肿和血管渗漏，口服EAG（50至500毫克/千克）预处理可显著减轻这些症状。巴豆油显著提高白细胞介素（IL）-6和PGE2的血液水平，但不影响肿瘤坏死因子（TNF）-α和一氧化氮（NO）水平。EAG预处理可显著降低IL-6和PGE2，但不改变TNF-α或NO浓度。这些结果表明，EAG部分通过阻断COX - PGE2途径减轻炎症反应。因此，EAG可能是治疗炎症性疾病的有前途的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/6a808873cfae/jvs-11-43-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/d4e58971c982/jvs-11-43-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/31ad245832c5/jvs-11-43-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/35bbaa403b07/jvs-11-43-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/6a808873cfae/jvs-11-43-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/d4e58971c982/jvs-11-43-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/31ad245832c5/jvs-11-43-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/35bbaa403b07/jvs-11-43-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54a2/2833429/6a808873cfae/jvs-11-43-g004.jpg

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