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干酪乳杆菌丙酸通过刺激 DSS 诱导的结肠炎大鼠模型肠杯状细胞中 MUC2 的表达来改善急性结肠炎。

Dairy Propionibacterium freudenreichii ameliorates acute colitis by stimulating MUC2 expression in intestinal goblet cell in a DSS-induced colitis rat model.

机构信息

Department of Integrated Biomedical and Life Sciences, Graduate School, Korea University, Seoul, 02841, Republic of Korea.

Department of Public Health Science (Brain Korea 21 PLUS program), Graduate School, Korea University, Seoul, 02841, Republic of Korea.

出版信息

Sci Rep. 2020 Mar 26;10(1):5523. doi: 10.1038/s41598-020-62497-8.

Abstract

An intact mucus layer is important in managing inflammatory bowel disease (IBD). Dairy Propionibacterium freudenreichii has probiotic potential, produces propionic acid and is known to promote health. The aim of this study was to evaluate the effects of P. freudenreichii on the improvement of colitis. LS 174T goblet cells and a dextran sodium sulfate (DSS)-induced colitis rat model were used to investigate the P. freudenreichii-induced stimulation of mucin production in vitro and in vivo, respectively. The mRNA and protein expression levels of MUC2, a main component of intestinal mucus, increased in the supernatant of P. freudenreichii culture (SPFC)-treated LS 174 cells. The SPFC and live P. freudenreichii (LPF) reduced the disease activity index (DAI) in the rats with DSS-induced colitis. After treatment with SPFC or LPF, the mRNA levels of typical pro-inflammatory cytokines decreased and the inflammatory state was histologically improved in the rats with DSS-induced colitis. The SPFC and LPF treatments increased the gene and protein expression levels of MUC2 in the rats with DSS-induced colitis compared with the expression levels in the negative control rats, and immunohistochemistry (IHC) showed an increase of the intestinal MUC2 level. In addition, SPFC and LPF augmented the level of propionate in the faeces of the rats with DSS-induced colitis. In conclusion, P. freudenreichii might improve acute colitis by restoring goblet cell number and stimulating the expression of MUC2 in intestinal goblet cells.

摘要

完整的黏液层对于管理炎症性肠病(IBD)很重要。干酪乳杆菌具有益生菌潜力,可产生丙酸,并被认为有助于健康。本研究旨在评估干酪乳杆菌对改善结肠炎的作用。LS174T 杯状细胞和葡聚糖硫酸钠(DSS)诱导的结肠炎大鼠模型分别用于体外和体内研究干酪乳杆菌诱导的黏蛋白产生的刺激作用。P. freudenreichii 培养上清(SPFC)处理的 LS174 细胞的上清液中,MUC2(肠道黏液的主要成分)的 mRNA 和蛋白表达水平增加。SPFC 和活干酪乳杆菌(LPF)降低了 DSS 诱导结肠炎大鼠的疾病活动指数(DAI)。用 SPFC 或 LPF 处理后,DSS 诱导结肠炎大鼠的典型促炎细胞因子的 mRNA 水平降低,炎症状态在组织学上得到改善。与阴性对照大鼠相比,SPFC 和 LPF 处理增加了 DSS 诱导结肠炎大鼠的 MUC2 基因和蛋白表达水平,免疫组织化学(IHC)显示肠道 MUC2 水平增加。此外,SPFC 和 LPF 增加了 DSS 诱导结肠炎大鼠粪便中丙酸的水平。总之,干酪乳杆菌可能通过恢复杯状细胞数量并刺激肠杯状细胞中 MUC2 的表达来改善急性结肠炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a5e/7099060/d1dafce53a05/41598_2020_62497_Fig1_HTML.jpg

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