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维生素K2通过炎症反应、肠道屏障完整性和小鼠肠道微生物群减轻葡聚糖硫酸钠诱导的结肠炎。

Vitamin K2 alleviates dextran sulfate sodium-induced colitis via inflammatory responses, gut barrier integrity, and the gut microbiota in mice.

作者信息

Wang Huakai, Liu Zhen, Zhan Kai, Ma Qiugang, Xu Lei, Li Yinghao, Liu Yun

机构信息

Anhui Provincial Key Laboratory of Livestock and Poultry Product Safety Engineering, Institute of Animal Husbandry and Veterinary Medicine, Anhui Academy of Agricultural Sciences, Hefei 230031, China.

Anhui Provincial Key Laboratory of Livestock and Poultry Product Safety Engineering, Institute of Animal Husbandry and Veterinary Medicine, Anhui Academy of Agricultural Sciences, Hefei 230031, China.

出版信息

Int J Biol Macromol. 2024 Nov;280(Pt 4):136091. doi: 10.1016/j.ijbiomac.2024.136091. Epub 2024 Sep 29.

Abstract

Vitamin K2 (VK2) has been shown to have potential benefits in improving intestinal integrity, but its potential and mechanisms for alleviating intestinal inflammation are still unclear. The present results showed that VK2 supplementation significantly alleviated the symptoms of colitis and maintained the intestinal barrier integrity. In addition, VK2 significantly down-regulated the mRNA expression levels of pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α, while up-regulated the mRNA expression level of anti-inflammatory cytokines such as IL-10. Moreover, VK2 significantly alleviated DSS-induced intestinal epithelial barrier dysfunction by maintaining the tight junction function. Furthermore, VK2 also regulated DSS-induced gut microbiota dysbiosis by reshaping the structure of gut microbiota, such as increasing the relative abundance of Firmicutes, Euryarchaeota, Prevotellaceae, and Prevotella and reducing the relative abundance of Proteobacteria, Rikenellaceae, Enterobacteriaceae, Acetatifactor, and Alistioes. In conclusion, these results indicated that VK2 effectively alleviates DSS-induced colitis in mice by modulating the gut microbiota.

摘要

维生素K2(VK2)已被证明在改善肠道完整性方面具有潜在益处,但其缓解肠道炎症的潜力和机制仍不清楚。目前的结果表明,补充VK2可显著减轻结肠炎症状并维持肠道屏障完整性。此外,VK2显著下调促炎细胞因子(包括IL-1β、IL-6和TNF-α)的mRNA表达水平,同时上调抗炎细胞因子(如IL-10)的mRNA表达水平。此外,VK2通过维持紧密连接功能显著减轻了右旋糖酐硫酸钠(DSS)诱导的肠道上皮屏障功能障碍。此外,VK2还通过重塑肠道微生物群结构来调节DSS诱导的肠道微生物群失调,例如增加厚壁菌门、广古菌门、普雷沃氏菌科和普雷沃氏菌属的相对丰度,并降低变形菌门、理研菌科、肠杆菌科、乙酸杆菌属和阿里斯托菌属的相对丰度。总之,这些结果表明VK2通过调节肠道微生物群有效减轻DSS诱导的小鼠结肠炎。

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