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通过激活Keap1/Nrf-2、改善肠道屏障功能和调节肠道微生物群来减轻硫酸葡聚糖钠诱导的大鼠溃疡性结肠炎。

Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Rats by Keap1/Nrf-2 Activation, Intestinal Barrier Function, and Gut Microbiota Regulation.

作者信息

Ma Xuewei, Hu Yichen, Li Xin, Zheng Xiaoting, Wang Yitao, Zhang Jinming, Fu Chaomei, Geng Funeng

机构信息

School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

College of Pharmacy and Biological Engineering, Chengdu University, Chengdu, China.

出版信息

Front Pharmacol. 2018 Aug 22;9:944. doi: 10.3389/fphar.2018.00944. eCollection 2018.

DOI:10.3389/fphar.2018.00944
PMID:30186174
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6113651/
Abstract

, a magic medicinal insect being present for over 300 million years, exhibits desirable therapeutic outcome for gastrointestinal ulcer treatment. Nowadays, ethanol extract (PAE) has been shown to ameliorate ulcerative colitis (UC) by either single-use or in combination with other therapeutic agents in clinics. However, its underlying mechanisms are still seldom known. Herein, we investigated the anti-UC activity of PAE by alleviating intestinal inflammation and regulating the disturbed gut microbiota structure in dextran sulfate sodium (DSS)-induced UC rats. Based on multiple constitute analyses by HPLC for quality control, PAE was administrated to DSS-induced UC rats by oral gavage for 2 weeks. The anti-UC effect of PAE was evaluated by inflammatory cytokine production, immunohistochemical staining, and gut microbiota analysis via 16S rRNA sequencing. As a result, PAE remarkably attenuated DSS-induced UC in rats. The colonic inflammatory responses manifested as decreased colonic atrophy, intestinal histopathology scores and inflammatory cytokines. In addition, PAE improved the intestinal barrier function via activating Keap1/Nrf-2 pathway and promoting the expressions of tight junction proteins. It was observed that the UC rats showed symptoms of gut microbial disturbance, i.e., the increased ratio and the significantly decreased probiotics such as , , and , which were negatively correlated with these detected pro-inflammatory cytokines (secreted by immune CD T cells, and including IFN-γ, TNF-α, IL-6, IL-8, IL-17, IL-1β). Besides, PAE administration regulated the abnormal intestinal microbial composition and made it similar to that in normal rats. Therefore, PAE could attenuate the DSS-induced UC in rats, by means of ameliorating intestinal inflammation, improving intestinal barrier function, and regulating the disturbed gut microbiota, especially improving beneficial intestinal flora growth, modulating the flora structure, and restoring the intestinal-immune system.

摘要

作为一种已存在超过3亿年的神奇药用昆虫，对治疗胃肠道溃疡具有理想的治疗效果。如今，乙醇提取物（PAE）已被证明在临床上单独使用或与其他治疗药物联合使用时可改善溃疡性结肠炎（UC）。然而，其潜在机制仍鲜为人知。在此，我们通过减轻肠道炎症和调节葡聚糖硫酸钠（DSS）诱导的UC大鼠中紊乱的肠道微生物群结构，研究了PAE的抗UC活性。基于通过HPLC进行的多种成分分析以进行质量控制，将PAE通过口服灌胃给予DSS诱导的UC大鼠2周。通过炎症细胞因子产生、免疫组织化学染色以及通过16S rRNA测序进行的肠道微生物群分析来评估PAE的抗UC作用。结果，PAE显著减轻了DSS诱导的大鼠UC。结肠炎症反应表现为结肠萎缩、肠道组织病理学评分和炎症细胞因子降低。此外，PAE通过激活Keap1/Nrf-2途径并促进紧密连接蛋白的表达来改善肠道屏障功能。观察到UC大鼠表现出肠道微生物紊乱的症状，即[具体微生物名称1]、[具体微生物名称2]和[具体微生物名称3]等比例增加且益生菌显著减少，这些与检测到的促炎细胞因子（由免疫CD T细胞分泌，包括IFN-γ、TNF-α、IL-6、IL-8、IL-17、IL-1β）呈负相关。此外，给予PAE可调节异常的肠道微生物组成并使其与正常大鼠相似。因此，PAE可通过减轻肠道炎症、改善肠道屏障功能和调节紊乱的肠道微生物群，特别是促进有益肠道菌群生长、调节菌群结构和恢复肠道免疫系统，来减轻DSS诱导的大鼠UC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/e206ff3bf946/fphar-09-00944-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/a654a8b83de5/fphar-09-00944-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/e206ff3bf946/fphar-09-00944-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/5247ac72c274/fphar-09-00944-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/ca365c8b6cc1/fphar-09-00944-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/2ac845d9da0b/fphar-09-00944-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66b0/6113651/a654a8b83de5/fphar-09-00944-g007.jpg
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