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给予……可抑制结肠5-羟色胺的增加,并减轻葡聚糖硫酸钠诱导的小鼠结肠炎的症状。 (你提供的原文中“Administration of ”后面应该还有具体物质,这里只是按完整句式给出翻译)

Administration of suppresses the increase of colonic serotonin and alleviates symptoms in dextran sodium sulfate-induced colitis in mice.

作者信息

Tatsuoka Misa, Shimada Riku, Ohsaka Fumina, Sonoyama Kei

机构信息

Graduate School of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kita-ku, Sapporo 060-8589, Japan.

Laboratory of Food Biochemistry, Research Faculty of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kita-ku, Sapporo 060-8589, Japan.

出版信息

Biosci Microbiota Food Health. 2023;42(3):186-194. doi: 10.12938/bmfh.2022-073. Epub 2023 Feb 28.

DOI:10.12938/bmfh.2022-073
PMID:37404566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10315192/
Abstract

Previous studies suggested that altered gut serotonin (5-HT) signaling is implicated in the pathophysiology of inflammatory bowel disease (IBD). Indeed, 5-HT administration reportedly exacerbated the severity of murine dextran sodium sulfate (DSS)-induced colitis that mimics human IBD. Our recent study suggested that , one of the most predominant bifidobacterial species in various mammals, reduces the colonic 5-HT content in mice. The present study thus tested whether the administration of prevents DSS-induced colitis in mice. Colitis was induced by administering 3% DSS in drinking water in female BALB/c mice, and (10 CFU/day) or 5-aminosalicylic acid (5-ASA, 200 mg/kg body weight) was intragastrically administered once daily throughout the experimental period. administration reduced body weight loss, diarrhea, fecal bleeding, colon shortening, spleen enlargement, and colon tissue damage and increased colonic mRNA levels of cytokine genes (, , , and ) almost to an extent similar to 5-ASA administration in DSS-treated mice. administration also reduced the increase of colonic 5-HT content, whereas it did not alter the colonic mRNA levels of genes that encode the 5-HT synthesizing enzyme, 5-HT reuptake transporter, 5-HT metabolizing enzyme, and tight junction-associated proteins. We propose that is as beneficial against murine DSS-induced colitis as the widely used anti-inflammatory agent 5-ASA. However, further studies are needed to clarify the causal relationship between the reduced colonic 5-HT content and reduced severity of DSS-induced colitis caused by administration.

摘要

先前的研究表明,肠道5-羟色胺(5-HT)信号改变与炎症性肠病(IBD)的病理生理学有关。事实上,据报道,给予5-HT会加剧小鼠葡聚糖硫酸钠(DSS)诱导的结肠炎的严重程度,该结肠炎可模拟人类IBD。我们最近的研究表明,作为各种哺乳动物中最主要的双歧杆菌种类之一,可降低小鼠结肠中的5-HT含量。因此,本研究测试了给予是否能预防小鼠DSS诱导的结肠炎。通过在雌性BALB/c小鼠的饮用水中给予3% DSS来诱导结肠炎,并在整个实验期间每天一次胃内给予(10 CFU/天)或5-氨基水杨酸(5-ASA,200 mg/kg体重)。给予可减轻体重减轻、腹泻、粪便出血、结肠缩短、脾脏肿大和结肠组织损伤,并使细胞因子基因(、、、和)的结肠mRNA水平增加,其程度几乎与DSS处理小鼠中给予5-ASA相似。给予还可降低结肠5-HT含量的增加,而它并未改变编码5-HT合成酶、5-HT再摄取转运体、5-HT代谢酶和紧密连接相关蛋白的基因的结肠mRNA水平。我们提出,与广泛使用的抗炎药物5-ASA一样,对小鼠DSS诱导的结肠炎有益。然而,需要进一步研究来阐明结肠5-HT含量降低与给予导致的DSS诱导的结肠炎严重程度降低之间的因果关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/6d2e9ef7bfe5/bmfh-42-186-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/b230dfea2e89/bmfh-42-186-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/03941181153e/bmfh-42-186-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/dc80488fba73/bmfh-42-186-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/54e37ecefc86/bmfh-42-186-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/974dfb96e0d1/bmfh-42-186-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/6d2e9ef7bfe5/bmfh-42-186-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/b230dfea2e89/bmfh-42-186-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/03941181153e/bmfh-42-186-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/dc80488fba73/bmfh-42-186-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/54e37ecefc86/bmfh-42-186-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/974dfb96e0d1/bmfh-42-186-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44ba/10315192/6d2e9ef7bfe5/bmfh-42-186-g006.jpg

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