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垂盆草通过调节肠道上皮细胞的炎症反应改善 DSS 诱导的结肠炎。

Eclipta prostrata Improves DSS-Induced Colitis through Regulation of Inflammatory Response in Intestinal Epithelial Cells.

机构信息

* Department of Oriental Pharmacy, College of Pharmacy, Wonkwnag University, Iksan, Jeonbuk 54538, Republic of Korea.

† Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Dongdaemun-gu, Seoul 02453, Republic of Korea.

出版信息

Am J Chin Med. 2017;45(5):1047-1060. doi: 10.1142/S0192415X17500562. Epub 2017 Jun 28.

Abstract

Eclipta prostrata (EP) and its compounds are known to have several pharmacological effects including anti-inflammatory effects. In the present study, we demonstrated that EP improves the dextran sulfate sodium (DSS)-induced colitis symptoms such as body weight loss, colon length shortening and disease activity index. In DSS-induced colitis tissue, EP controls the protein expressions of cyclooxygenase-2 (COX-2) and hypoxia inducible factor-1[Formula: see text] (HIF-1[Formula: see text]). In addition, the release of prostaglandin E and vascular endothelial growth factor-A were significantly reduced by EP administration. EP also inhibited COX-2 and HIF-1[Formula: see text] expressions in the tumor necrosis factor-[Formula: see text] stimulated HT-29 cells. These inhibitory effects of EP occurred by reducing the phosphorylation of I[Formula: see text]B and the translocation of the nuclear factor-[Formula: see text]B (NF-[Formula: see text]B). Additionally, we found through HPLC analysis that wedelolactone, which is an inhibitor of NF-[Formula: see text]B transcription, was contained in water extract of EP. These results indicate that EP can improve colitis symptoms through the modulation of immune function in intestinal epithelial cells and suggests that EP has the potential therapeutic effect to intestinal inflammation.

摘要

旱莲草(EP)及其化合物已知具有多种药理作用,包括抗炎作用。在本研究中,我们证明 EP 可改善葡聚糖硫酸钠(DSS)诱导的结肠炎症状,如体重减轻、结肠缩短和疾病活动指数。在 DSS 诱导的结肠炎组织中,EP 控制环氧化酶-2(COX-2)和缺氧诱导因子-1[公式:见文本](HIF-1[公式:见文本])的蛋白表达。此外,EP 给药可显著减少前列腺素 E 和血管内皮生长因子-A 的释放。EP 还抑制肿瘤坏死因子-[Formula: see text]刺激的 HT-29 细胞中 COX-2 和 HIF-1[Formula: see text]的表达。EP 的这些抑制作用通过减少 I[Formula: see text]B 的磷酸化和核因子-[Formula: see text]B(NF-[Formula: see text]B)的易位发生。此外,我们通过 HPLC 分析发现,wedelolactone 是 NF-[Formula: see text]B 转录的抑制剂,存在于 EP 的水提取物中。这些结果表明,EP 可以通过调节肠上皮细胞的免疫功能来改善结肠炎症状,并表明 EP 具有治疗肠道炎症的潜在疗效。

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