Alpha-lipoic acid preconditioning plus ischemic postconditioning provides additional protection against myocardial reperfusion injury of diabetic rats: modulation of autophagy and mitochondrial function
| العنوان: | Alpha-lipoic acid preconditioning plus ischemic postconditioning provides additional protection against myocardial reperfusion injury of diabetic rats: modulation of autophagy and mitochondrial function |
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| المؤلفون: | Behnaz Mokhtari, Mahdi Abdoli-Shadbad, Alireza Alihemmati, Aniseh Javadi, Reza Badalzadeh |
| المصدر: | Molecular Biology Reports. 49:1773-1782 |
| بيانات النشر: | Springer Science and Business Media LLC, 2022. |
| سنة النشر: | 2022 |
| مصطلحات موضوعية: | Thioctic Acid, Ischemic Preconditioning, Myocardial, Autophagy, Genetics, Animals, Myocardial Reperfusion Injury, General Medicine, Ischemic Postconditioning, Molecular Biology, Diabetes Mellitus, Experimental, Mitochondria, Rats |
| الوصف: | Investigating the interaction of diabetes with ischemic postconditioning (IPostC)-associated cardioprotection in myocardial ischemia/reperfusion (I/R) damage is of great clinical importance. The present work was designed to determine the possible synergistic effects of alpha-lipoic acid (LA) preconditioning and IPostC on myocardial I/R damage in type-II diabetic rats through modulating autophagy, and the involvement of mitochondrial function.High-fat diet/low dose of streptozotocin-induced type-II diabetic model with duration of 12 weeks was used in this study. LA (100 mg/kg/day) was administered orally in diabetic rats for 5 weeks before I/R. Myocardial I/R was established on Langendorff apparatus through the ligation of left anterior descending coronary artery for 35 min, then reperfusion for 60 min. IPostC was carried out immediately at the beginning of the reperfusion. At the end of the experiment, myocardial infarct size (IS), autophagy markers at both gene and protein levels, and mitochondrial ROS production and membrane potential were assessed.Combined conditioning with LA and ischemia significantly decreased the IS of diabetic hearts (P0.05), however, single therapies had no significant effects. LA in combination with IPostC more significantly decreased LC3 and p62 mRNA levels (P0.01), and LC3II/LC3I and p62 protein levels (P0.01). Also, this combined therapy decreased mitochondrial ROS generation and membrane depolarization (P0.01).Pretreatment with LA in diabetic rats notably restored cardioprotection by IPostC via modulating autophagy and restoring mitochondrial function. This combined conditioning might be an effective strategy to diminish I/R damage in diabetic hearts. |
| تدمد: | 1573-4978 0301-4851 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::76f696e918a308a96714961536e005f1Test https://doi.org/10.1007/s11033-021-06987-6Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....76f696e918a308a96714961536e005f1 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15734978 03014851 |
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