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(树名)树叶乙醇提取物对葡聚糖硫酸钠诱导的小鼠溃疡性结肠炎的抗炎作用。

Anti-inflammatory effects of ethanolic extract from ( Tree) leaves in mice with dextran sulfate sodium-induced ulcerative colitis.

作者信息

Moon Hye-Jung, Cha Youn-Soo, Kim Kyung-Ah

机构信息

Department of Food Science and Human Nutrition, Jeonbuk National University, Jeonju, Republic of Korea.

K-Food Research Center, Jeonju, Republic of Korea.

出版信息

Food Nutr Res. 2025 Jul 21;69. doi: 10.29219/fnr.v69.11052. eCollection 2025.

Abstract

(Miseon tree), a native Korean plant, is known for the high phenolic content in its leaves. The ethanolic leaf extracts of have shown antioxidant, anti-obesity, and anti-inflammatory properties. However, studies on its potential to improve colitis are limited. This study aimed to determine whether the ethanolic extract of leaves (ADE) could alleviate dextran sulfate sodium (DSS)-induced colitis in mice. The mice were divided into three groups, and the experimental group was given 300 mg/kg ADE for 4 weeks. One week before the end of the experiment, 3% DSS was added to the drinking water to induce colitis. The clinical symptoms of colitis and damage to colon tissue, including the increase in abundance and a decrease in in the colon, were evaluated during DSS treatment. DSS overactivated the nuclear factor (NF)-κB signaling pathway, resulting in excessive production of pro-inflammatory cytokines. In contrast, ADE alleviated the DSS-induced colitis symptoms, protected against colonic tissue damage, and restored the balance of and levels in the colon. Moreover, ADE effectively inhibited the DSS-induced overactivation of the NF-κB signaling pathway within the colon and mitigated abnormal inflammatory responses. These findings suggest that ADE protects against colitis by modulating the growth of some intestinal strains and the NF-κB pathway in the colon, supporting its potential as a natural agent.

摘要

米森树是一种韩国本土植物,以其叶片中高含量的酚类物质而闻名。其乙醇叶提取物已显示出抗氧化、抗肥胖和抗炎特性。然而,关于其改善结肠炎潜力的研究有限。本研究旨在确定米森树叶乙醇提取物(ADE)是否能减轻葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎。将小鼠分为三组,实验组给予300mg/kg ADE,持续4周。在实验结束前一周,向饮用水中添加3% DSS以诱导结肠炎。在DSS治疗期间评估结肠炎的临床症状和结肠组织损伤,包括结肠中 丰度的增加和 含量的降低。DSS过度激活核因子(NF)-κB信号通路,导致促炎细胞因子过度产生。相比之下,ADE减轻了DSS诱导的结肠炎症状,保护结肠组织免受损伤,并恢复了结肠中 和 水平的平衡。此外,ADE有效抑制了结肠内DSS诱导的NF-κB信号通路过度激活,并减轻了异常炎症反应。这些发现表明,ADE通过调节结肠中某些肠道菌株的生长和NF-κB途径来预防结肠炎,支持其作为天然药物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c201/12320766/0f07c87216c3/FNR-69-11052-g001.jpg

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