Apigenin remodels the gut microbiota to ameliorate ulcerative colitis.
Apigenin remodels the gut microbiota to ameliorate ulcerative colitis.
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芹菜素重塑肠道微生物群以改善溃疡性结肠炎
DOI：
10.3389/fnut.2022.1062961
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发表时间：
2022
影响因子：
5
通讯作者：
Zhang, Min
中科院分区：
文献类型：
--
作者：
Fu, Rongrong;Wang, Lechen;Meng, Ying;Xue, Wenqing;Liang, Jingjie;Peng, Zimu;Meng, Jing;Zhang, Min
前言溃疡性结肠炎(UC)是一种病因不明的慢性非特异性结肠炎性疾病，长期困扰人类健康。肠道微生物区系失调破坏了结肠的内环境平衡，与溃疡性结肠炎的进展密切相关。芹菜素是一种广泛存在于芹菜中的黄酮类化合物，已被发现可以改善溃疡性结肠炎。然而，芹菜素通过保护肠道屏障和调节肠道微生物区系来改善溃疡性结肠炎的潜在分子机制仍不清楚。方法采用葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎模型，观察芹菜素对UC的影响。采用小鼠疾病活动指数评分、结肠组织病理学、细胞因子分析、肠道紧密连接蛋白表达、结肠内容物短链脂肪酸(SCFAs)和16S rRNA基因测序等方法反映芹菜素对UC的保护作用。结果芹菜素可明显减轻肠道病理损伤，增加杯状细胞数量和粘蛋白分泌，促进抗炎细胞因子IL-10的表达，抑制促炎细胞因子、肿瘤坏死因子-α、IL-1β、IL-6的表达和结肠组织髓过氧化物酶活性。芹菜素增加ZO-1、claudin-1和occludin的表达，以恢复肠屏障的完整性。此外，芹菜素通过调节Akkermansia、Turicibacter、Klebsiella、Romboutsia等及其代谢产物(SCFA)的丰度，重塑紊乱的肠道微生物区系，减轻DSS诱导的结肠损伤。我们还研究了补充芹菜素对肠道微生物区系潜在代谢途径的影响。结论芹菜素通过平衡肠道微生物区系，抑制炎症反应，保护肠道屏障，有效地改善DSS诱导的UC。芹菜素具有低毒、高效的特点，可通过调节宿主与微生物之间的相互作用和作用机制，成为治疗UC的潜在治疗策略。
Introduction Ulcerative colitis (UC), a chronic non-specific colorectal inflammatory disease with unclear etiology, has long plagued human health. Gut microbiota dysbiosis destroy homeostasis of the colon, which is closely related to ulcerative colitis progress. Apigenin, a flavonoid widely present in celery, has been found to improve ulcerative colitis. However, the potential molecular mechanism of apigenin ameliorating ulcerative colitis through protecting intestinal barrier and regulating gut microbiota remains undefined. Methods Dextran sodium sulfate (DSS)-induced colitis mouse model was conducted to evaluate the effect of apigenin on UC. Disease activity index score of mice, colon tissue pathological, cytokines analysis, intestinal tight junction proteins expression, and colonic content short-chain fatty acids (SCFAs) and 16S rRNA gene sequencing were conducted to reflect the protection of apigenin on UC. Results The results indicated that apigenin significantly relieved the intestinal pathological injury, increased goblet cells quantity and mucin secretion, promoted anti-inflammatory cytokines IL-10 expression, and inhibited the expression of proinflammatory cytokines, TNF-α, IL-1β, IL-6 and MPO activity of colon tissue. Apigenin increased ZO-1, claudin-1 and occludin expressions to restore the integrity of the intestinal barrier. Moreover, apigenin remodeled the disordered gut microbiota by regulating the abundance of Akkermansia, Turicibacter, Klebsiella, Romboutsia, etc., and its metabolites (SCFAs), attenuating DSS-induced colon injury. We also investigated the effect of apigenin supplementation on potential metabolic pathways of gut microbiota. Conclusion Apigenin effectively ameliorated DSS-induced UC via balancing gut microbiome to inhibit inflammation and protect gut barrier. With low toxicity and high efficiency, apigenin might serve as a potential therapeutic strategy for the treatment of UC via regulating the interaction and mechanism between host and microorganism.
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影响因子：
4.6
作者：
Bian S;Wan H;Liao X;Wang W
通讯作者：
Wang W
DOI：
10.1038/nri.2016.88
发表时间：
2016-10
期刊：
Nature reviews. Immunology
影响因子：
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作者：
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通讯作者：
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作者：
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影响因子：
29.4
作者：
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通讯作者：
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影响因子：
9.3
作者：
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通讯作者：
Si, Hongbin