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Clostridium butyricum protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis

  • Authors:
    • Miao Liu
    • Wenjie Xie
    • Xinyue Wan
    • Tao Deng
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    Affiliations: Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Central Laboratory of Renmin Hospital, Wuhan, Hubei 430060, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 10
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    Published online on: August 25, 2020
       https://doi.org/10.3892/etm.2020.9138
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Abstract

Clostridium butyricum (CB), a probiotic, is a gram‑positive obligate anaerobic bacillus with acid and heat resistant properties. Previous studies have reported that CB has beneficial effects in intestinal diseases and regulates intestinal function. The aim of the present study was to investigate the protective effects and mechanisms of CB on the intestinal barrier function. Mice were randomly divided into three experimental groups (n=15 mice/group), including control, dextran sodium sulfate (DSS) and DSS + CB. In the DSS and DSS + CB groups colitis was induced with 3% DSS dissolved in drinking water for 7 days. DSS + CB group mice were co‑treated daily with 200 µl (2x108 CFU) CB solution via gavage. The intestinal mucosal barrier function in mice was assessed by measuring FITC‑labeled 4‑kDa dextran (molecular weight, 4,000 Da) flux and by analyzing the expression of tight junction (TJ)‑related proteins using western blot analysis. In addition, the secretion levels of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β, IL‑6, IL‑10 and IL‑13, and the concentration of malondialdehyde, glutathione and superoxide dismutase were detected using ELISAs to determine inflammation and oxidative stress, respectively. The activation status of the Akt/mTOR signaling pathway was also investigated using western blot analysis. The results demonstrated that, in mice with DSS‑induced colitis treatment, co‑treatment with CB attenuated colitis symptoms and intestinal permeability, increased the expression levels of TJ‑related proteins, decreased TNF‑α, IL‑1β and IL‑13 secretion levels but increased those of IL‑10, and reduced oxidative stress. Additionally, CB elevated the phosphorylation of Akt, mTOR and p70 ribosomal protein S6 kinase. Collectively, the present results indicated that CB protected intestinal barrier function and decreased intestinal mucosal permeability via upregulating the expression levels of TJ‑related proteins in a mouse model of DSS‑induced colitis. Moreover, the results suggested that the effects of CB could be mediated by the Akt/mTOR signaling pathway.
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Spandidos Publications style
Liu M, Xie W, Wan X and Deng T: <em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis. Exp Ther Med 20: 10, 2020.
APA
Liu, M., Xie, W., Wan, X., & Deng, T. (2020). <em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis. Experimental and Therapeutic Medicine, 20, 10. https://doi.org/10.3892/etm.2020.9138
MLA
Liu, M., Xie, W., Wan, X., Deng, T."<em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis". Experimental and Therapeutic Medicine 20.5 (2020): 10.
Chicago
Liu, M., Xie, W., Wan, X., Deng, T."<em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis". Experimental and Therapeutic Medicine 20, no. 5 (2020): 10. https://doi.org/10.3892/etm.2020.9138
Copy and paste a formatted citation
x
Spandidos Publications style
Liu M, Xie W, Wan X and Deng T: <em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis. Exp Ther Med 20: 10, 2020.
APA
Liu, M., Xie, W., Wan, X., & Deng, T. (2020). <em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis. Experimental and Therapeutic Medicine, 20, 10. https://doi.org/10.3892/etm.2020.9138
MLA
Liu, M., Xie, W., Wan, X., Deng, T."<em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis". Experimental and Therapeutic Medicine 20.5 (2020): 10.
Chicago
Liu, M., Xie, W., Wan, X., Deng, T."<em>Clostridium&nbsp;butyricum</em> protects intestinal barrier function via upregulation of tight junction proteins and activation of the Akt/mTOR signaling pathway in a mouse model of dextran sodium sulfate‑induced colitis". Experimental and Therapeutic Medicine 20, no. 5 (2020): 10. https://doi.org/10.3892/etm.2020.9138
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