The probiotic Lacticaseibacillus rhamnosus SD11 alleviates the progression of liver and colon damage through modulation of inflammation and tight junction proteins in streptozotocin-induced diabetic mice.

Autor: Ruathong W; Faculty of Science, Division of Health and Applied Sciences, Prince of Songkla University, Songkhla, Thailand., Khuituan P; Faculty of Science, Division of Health and Applied Sciences, Prince of Songkla University, Songkhla, Thailand., Peerakietkhajorn S; Faculty of Science, Division of Biological Science, Prince of Songkla University, Songkhla, Thailand., Teanpaisan R; Faculty of Dentistry, Research Center of Excellence for Oral Health, Prince of Songkla University, Hat Yai, Thailand., Nopparat J; Faculty of Science, Division of Health and Applied Sciences, Prince of Songkla University, Songkhla, Thailand.; Center of Excellence for Trace Analysis and Biosensor, Prince of Songkla University, Hat Yai, Songkhla, Thailand.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2024 Nov 21; Vol. 19 (11), pp. e0313395. Date of Electronic Publication: 2024 Nov 21 (Print Publication: 2024).
DOI: 10.1371/journal.pone.0313395
Abstrakt: Lacticaseibacillus rhamnosus SD11 (SD11) has several health benefits for the host, including antidiabetic, anti-inflammatory, and antimicrobial effects. However, the antidiabetic mechanism of SD11 has not been clearly elucidated. The current study assessed the effects of SD11 and the associated underlying mechanisms on streptozotocin (STZ)-induced diabetic mice. Compared with the normal control, SD11 supplementation for 4 weeks significantly improved the metabolic profiles, including body weight (BW), fasting blood glucose (FBG), fasting insulin level (FIN), and liver index (LI), in conjunction with a lower NAS score. A notable reduction in the liver function parameters aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) and total cholesterol (TC), together with histopathology studies, supported diabetic recovery by SD11. A closer examination of two major markers for the insulin pathway, insulin receptor (INSR) and insulin substrate (IRS)-1, revealed that SD11 could exert its glucose control through the upregulation of these molecules, which were almost demolished in nontreated diabetic livers. Additionally, SD11-treated mice exhibited alleviation of oxidative stress enzymes; downregulation of proinflammatory cytokines, including interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ; and decreased infiltration of macrophages into liver tissue. These findings were concomitant with the preservation of the tight junction proteins occludin and zona occludin (ZO)-1, which in turn lowered the levels of the inflammatory cytokines IL-1β and TNF-α and prevented colon tissue injury to some extent. Notably, the results for the SD11 control mice were identical to those for the normal control mice. Overall, our findings that SD11 delays liver deterioration and reduces colon lesions in diabetic mice provide evidence for the use of SD11 as an effective strategy to improve diabetes-related symptoms.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Ruathong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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