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茯砖茶对葡聚糖硫酸钠诱导的C57BL/6小鼠结肠炎及肠源性肝损伤的保护机制

Protective Mechanism of from Fuzhuan Brick Tea against Colitis and Gut-Derived Liver Injury Induced by Dextran Sulfate Sodium in C57BL/6 Mice.

作者信息

Wang Xin, Liu Jinhu, Wei Jianping, Zhang Yuxiang, Xu Yunpeng, Yue Tianli, Yuan Yahong

机构信息

College of Health Management, Shangluo University, Shangluo 726000, China.

Shaanxi Union Research Center of University and Enterprise for Healthy and Wellness Industry, Shangluo 726000, China.

出版信息

Nutrients. 2024 Apr 16;16(8):1178. doi: 10.3390/nu16081178.

DOI:10.3390/nu16081178
PMID:38674869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11054642/
Abstract

The study explored the potential protective impact of the probiotic fungus in Fuzhuan brick tea on ulcerative colitis, along with the underlying mechanism. A spore suspension of was administered to C57BL/6 mice to alleviate DSS-induced colitis. The findings indicated that administering evidently enhanced the ultrastructure of colonic epithelium, showing characteristics such as enhanced TJ length, reduced microvilli damage, and enlarged intercellular space. After HLL supplementation, the activation of the liver inflammation pathway, including TLR4/NF-kB and NLRP3 inflammasome caused by DSS, was significantly suppressed, and bile acid metabolism, linking liver and gut, was enhanced, manifested by restoration of bile acid receptor (FXR, TGR5) level. The dysbiosis of the gut microbes in colitis mice was also restored by HLL intervention, characterized by the enrichment of beneficial bacteria (, , , and ) and fungi (, , , , and ), which was closely associated with lipid metabolism and amino acid metabolism, and was negatively correlated with inflammatory gene expression. Hence, the recovery of gut microbial community structure, implicated deeply in the inflammatory index and metabolites profile, might play a crucial role in the therapeutic mechanism of HLL on colitis.

摘要

该研究探讨了茯砖茶中益生菌真菌对溃疡性结肠炎的潜在保护作用及其潜在机制。将[具体益生菌真菌名称]的孢子悬浮液给予C57BL/6小鼠以减轻右旋糖酐硫酸钠(DSS)诱导的结肠炎。研究结果表明,给予[具体益生菌真菌名称]明显改善了结肠上皮的超微结构,表现为紧密连接长度增加、微绒毛损伤减少和细胞间隙增大。补充[具体益生菌真菌名称]后,由DSS引起的肝脏炎症途径(包括TLR4/NF-κB和NLRP3炎性小体)的激活受到显著抑制,连接肝脏和肠道的胆汁酸代谢增强,表现为胆汁酸受体(FXR、TGR5)水平的恢复。[具体益生菌真菌名称]干预还恢复了结肠炎小鼠肠道微生物群的失调,其特征是有益细菌([具体细菌名称]、[具体细菌名称]、[具体细菌名称]和[具体细菌名称])和真菌([具体真菌名称]、[具体真菌名称]、[具体真菌名称]、[具体真菌名称]和[具体真菌名称])的富集,这与脂质代谢和氨基酸代谢密切相关,与炎症基因表达呈负相关。因此,肠道微生物群落结构的恢复与炎症指标和代谢产物谱密切相关,可能在[具体益生菌真菌名称]对结肠炎的治疗机制中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/217f291fcb14/nutrients-16-01178-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/98bf37a31000/nutrients-16-01178-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/c4aef4dcffef/nutrients-16-01178-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/1159301c34bc/nutrients-16-01178-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/a9d26c837918/nutrients-16-01178-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/8b953b459099/nutrients-16-01178-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/da9072a01b82/nutrients-16-01178-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/217f291fcb14/nutrients-16-01178-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/98bf37a31000/nutrients-16-01178-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/c4aef4dcffef/nutrients-16-01178-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/1159301c34bc/nutrients-16-01178-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/a9d26c837918/nutrients-16-01178-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/8b953b459099/nutrients-16-01178-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/da9072a01b82/nutrients-16-01178-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b63c/11054642/217f291fcb14/nutrients-16-01178-g007.jpg

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