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Hyperglycemia-Induced Cardiac Damage Is Alleviated by Heat-Inactivated Lactobacillus reuteri GMNL-263 via Activation of the IGF1R Survival Pathway
Diabetes-induced cardiomyocyte apoptosis is one of the major causes of mortality in patients with diabetes. Numerous studies have indicated the beneficial effects of Lactobacillus reuteri GMNL-263. However, the protective effect of Lactobacillus reuteri GMNL-263 in cardiac damage associated with dia...
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Published in: | Probiotics and antimicrobial proteins 2021-08, Vol.13 (4), p.1044-1053 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Diabetes-induced cardiomyocyte apoptosis is one of the major causes of mortality in patients with diabetes. Numerous studies have indicated the beneficial effects of
Lactobacillus reuteri
GMNL-263. However, the protective effect of
Lactobacillus reuteri
GMNL-263 in cardiac damage associated with diabetes remains poorly understood. In this study, we aimed to investigate the protective effect of
Lactobacillus reuteri
GMNL-263 on cardiomyocytes in diabetic rats. Five-week-old male Wistar rats were categorized into normal control group, diabetes group (55 mg/kgw STZ-induced diabetes via intraperitoneal injection), and diabetic animals treated with
Lactobacillus reuteri
GMNL-263 (10
9
CFU/rat/day, oral administration for 4 weeks). The results were presented that oral administration of a high dose of
Lactobacillus reuteri
GMNL-263 in diabetic rats activated IGF1R cell survival pathways to decrease the Fas-dependent and mitochondrial-dependent apoptotic pathways induced by hyperglycemia. We found that GMNL-263 significantly attenuated cell apoptosis via the IGF1R survival pathway in diabetic rats. The findings of this study suggest that GMNL-263 treatment maybe an effective therapeutic approach for the prevention of cardiac apoptosis in patients with diabetes.
Graphical abstract |
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ISSN: | 1867-1306 1867-1314 |
DOI: | 10.1007/s12602-021-09745-z |