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苦参甲醇提取物(苦丁茶 C.J. Tseng)对葡聚糖硫酸钠诱导的溃疡性结肠炎的抗炎作用。

Anti-inflammatory effects of kudingcha methanol extract (Ilex kudingcha C.J. Tseng) in dextran sulfate sodium-induced ulcerative colitis.

机构信息

Department of Food Science and Nutrition, Pusan National University, Busan 609-735, Republic of Korea.

出版信息

Mol Med Rep. 2013 Oct;8(4):1256-62. doi: 10.3892/mmr.2013.1635. Epub 2013 Aug 14.

Abstract

The present study aimed to investigate the anti‑inflammatory effects of Ilex kudingcha C.J. Tseng methanol extracts (KME) on 3% dextran sulfate sodium (DSS)‑induced ulcerative colitis (UC) in mice (C57BL/6J strain). Body weight, disease activity index (DAI), colon length, colon weight to length ratio, colonic myeloperoxidase (MPO), glutathione (GSH) and malondialdehyde (MDA) levels were measured. Histological changes were observed by hematoxylin and eosin staining. Colonic levels of tumor necrosis factor‑α (TNF‑α), interleukin(IL)‑1β and IL‑6 were measured with an enzyme‑linked immunosorbent assay. The mRNA expression of TNF‑α, IL‑1β, ‑6, inducible nitric oxide synthase (iNOS) and cyclooxygenase‑2 (COX-2) in the colon tissue, was quantified by RT‑PCR. KME significantly suppressed DSS‑induced body weight loss, colon length shortening and decreased the colon weight to length ratio. It also resulted in increased GSH and reduced MPO and MDA levels in the colon tissue. Histological observation suggested that KME prevented edema, mucosal damage and loss of crypts, which are induced by DSS. In addition, KME decreased the levels of TNF‑α, IL‑1β and ‑6 in the colon tissues, while inhibiting the mRNA expression of these cytokines, as well as iNOS and COX‑2. The results of this study suggested that KME has anti‑inflammatory effects on DSS‑induced UC in mice (C57BL/6J strain) by reducing the colonic levels and inhibiting the mRNA expression of pro‑inflammatory cytokines.

摘要

本研究旨在探讨苦丁茶甲醇提取物(KME)对 3%葡聚糖硫酸钠(DSS)诱导的 C57BL/6J 小鼠溃疡性结肠炎(UC)的抗炎作用。测量体重、疾病活动指数(DAI)、结肠长度、结肠长度与体重比、结肠髓过氧化物酶(MPO)、谷胱甘肽(GSH)和丙二醛(MDA)水平。通过苏木精和伊红染色观察组织学变化。采用酶联免疫吸附试验测定结肠组织中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β和 IL-6 的水平。采用 RT-PCR 定量测定结肠组织中 TNF-α、IL-1β、IL-6、诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的 mRNA 表达。KME 显著抑制 DSS 诱导的体重减轻、结肠缩短和结肠长度与体重比降低。还导致结肠组织中 GSH 增加,MPO 和 MDA 水平降低。组织学观察表明,KME 可预防 DSS 诱导的水肿、粘膜损伤和隐窝丢失。此外,KME 降低了结肠组织中 TNF-α、IL-1β 和 IL-6 的水平,同时抑制了这些细胞因子以及 iNOS 和 COX-2 的 mRNA 表达。本研究结果表明,KME 通过降低结肠水平和抑制促炎细胞因子的 mRNA 表达,对 DSS 诱导的 C57BL/6J 小鼠 UC 具有抗炎作用。

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