Orally Administered Lactobacillus rhamnosus CY12 Alleviates DSS-Induced Colitis in Mice by Restoring the Intestinal Barrier and Inhibiting the TLR4-MyD88-NF-κB Pathway via Intestinal Microbiota Modulation

文献类型： 外文期刊

第一作者： Zheng, Juanshan

作者： Zheng, Juanshan;Ahmad, Anum Ali;Yang, Chen;Liang, Zeyi;Liu, Jing;Ding, Xuezhi;Zheng, Juanshan;Ahmad, Anum Ali;Yang, Chen;Liang, Zeyi;Liu, Jing;Ding, Xuezhi;Zheng, Juanshan;Lan, Xianyong;Ahmad, Anum Ali;Shen, Wenxiang;Yan, Zuoting;Yang, Yayuan;Dong, Pengcheng;Ding, Xuezhi;Han, Jianlin;Han, Jianlin;Salekdeh, Ghasem Hosseini

作者机构：

关键词： Lactobacillus rhamnosusCY12; inflammatory bowel diseases; short-chain fattyacids; gut microbiota; DSS-inducedcolitis

期刊名称：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY （ 影响因子：6.1； 五年影响因子：6.3 ）

ISSN： 0021-8561

年卷期： 2024 年 72 卷 16 期

页码：

收录情况： SCI

摘要： Oral ingestion of probiotics is a promising approach to relieving inflammatory disease through regulating the gut microbiota. A newly discovered strain, Lactobacillus rhamnosus CY12 (LCY12), obtained from cattle-yak milk, displayed numerous probiotic properties. These included enhanced viability in low pH and bile environments, adhesion capabilities, and potent antimicrobial effects. The research aimed to explore the beneficial impacts of the novel LCY12 strain on colitis in mice induced by dextran sulfate sodium (DSS) and to elucidate the underlying molecular mechanisms. The results of the study showed that administration of LCY12 effectively helped to reduce the negative effects of DSS-induced body weight loss, disease activity index score, colon length shortening, loss of goblet cells, and overall histopathological scores in the intestines. Simultaneously, LCY12 administration significantly alleviated intestinal inflammation and safeguarded intestinal barrier integrity by enhancing IL-10 levels, while dampening IL-6, IL-1 beta, and TNF-alpha production. Additionally, LCY12 boosted the presence of tight junction proteins. Furthermore, LCY12 hindered the TLR4/MyD88/NF-kappa B signaling pathway by downregulating TLR4 and MyD88 expression, inactivating phosphorylated I kappa B alpha, and preventing translocation of NF-kappa B p65 from the cytoplasm to the nucleus. The LCY12 also increased specific intestinal microbial communities and short-chain fatty acid (SCFA) production. Altogether, LCY12 oral administration alleviated colitis induced with DSS in mice by improving intestinal barrier function and regulating inflammatory cytokines, SCFA production, and intestinal microbiota.

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