Wei-Wen Kuo1,2, Chih-Yang Huang3,4,5,6,7, Chung-Jen Chiang8, Bruce Chi-Kang Tsai9, Tzu-Li Lu8, Yun-Peng Chao10, Cecilia Hsuan Day11, Tsung-Jung Ho12,13,14, Pin-Ning Wang10, Sheng-Chuan Lin8, V Vijaya Padma15. 1. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan. 2. Ph.D. Program for Biotechnology Industry, China Medical University, Taichung, Taiwan. 3. Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan. cyhuang@mail.cmu.edu.tw. 4. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw. 5. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw. 6. Department of Biological Science and Technology, Asia University, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw. 7. Center of General Education, Buddhist Tzu Chi Medical Foundation, Tzu Chi University of Science and Technology, Hualien, Taiwan. cyhuang@mail.cmu.edu.tw. 8. Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan. 9. Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan. 10. Department of Chemical Engineering, Feng Chia University, Taichung, Taiwan. 11. Department of Nursing, MeiHo University, Pingtung, Taiwan. 12. Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan. 13. Integration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan. 14. School of Post-Baccalaureate Chinese Medicine, College of Medicine, Tzu Chi University, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan. 15. Department of Biotechnology, Bharathiar University, Coimbatore, India.
Abstract
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.
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.
Authors: Heidi Yeh; Sarah A Skubel; Harna Patel; Denia Cai Shi; David Bushek; Michael L Chikindas Journal: Probiotics Antimicrob Proteins Date: 2020-06 Impact factor: 4.609