Purpose: Diabetes mellitus (DM) leads to disorders such as cardiac hypertrophy, cardiac myocyte apoptosis, and cardiac fibrosis. Previous studies have shown that Lactobacillus reuteri GMNL-263 decreases cardiomyopathy by reducing inflammation. In this study, we investigated the potential benefit of GMNL-263 supplementation in treating diabetes-induced cardiomyocytes in rats with DM.
Methods: Five-week-old male Wistar rats were randomly divided into three groups, control, DM, and rats with DM treated with different dosages of L. reuteri GMNL-263. After undergoing treatment for 4 weeks, all rats were euthanized for further analysis.
Results: We observed that cardiac function and structure of rats with DM was rescued by GMNL-263. Activation of toll-like receptor 4 (TLR4)-related inflammatory, hypertrophic, and fibrotic signaling pathways in the hearts of rats with DM was reduced by treatment with GMNL-263.
Conclusion: Our findings demonstrate that GMNL-263 inhibited diabetes-induced cardiomyocytes via the repression of the TLR4 pathway. Moreover, these findings suggest that treatment with high-dose GMNL-263 could be a precautionary therapy for reducing the diabetes-induced cardiomyopathy.
Keywords: Cardiomyopathy; Diabetes mellitus; GMNL-263; TGF-β; TLR4.
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