Cardioprotective effect of IGF-1 against myocardial ischemia/reperfusion injury through activation of PI3K/Akt pathway in rats
Autor: | Yaojun Liao, Hong Li, Yanna Pi, Zijia Li, Sanqing Jin |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: | |
Zdroj: | Journal of International Medical Research, Vol 47 (2019) |
Druh dokumentu: | article |
ISSN: | 0300-0605 1473-2300 03000605 |
DOI: | 10.1177/0300060519857839 |
Popis: | Objective It remains unknown whether insulin-like growth factor-1 (IGF-1) can attenuate myocardial ischemia/reperfusion (I/R) injury in vivo by activating the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway. This study investigated the possible interaction of IGF-1 with the PI3K/Akt pathway in cardioprotection against in vivo myocardial I/R injury in rats. Methods We established a myocardial I/R model in rats through left anterior descending artery ligation for 40 minutes followed by 6 hours reperfusion. The PI3K/Akt inhibitor, LY294002 (0.3 mg/kg), was injected through the caudal vein 30 minutes before myocardial ischemia, and IGF-1 (1 µg/kg or 5 µg/kg) was injected through the caudal vein 10 minutes before myocardial ischemia. Results IGF-1 treatment decreased myocardial infarct size; myocardial cell apoptosis; and serum lactate dehydrogenase, creatine kinase MB, and cardiac troponin I levels in rats with myocardial I/R in vivo . Moreover, IGF-1 treatment led to significant increases in expression levels of p-Akt (Ser473) and B cell lymphoma 2, while reducing expression levels of caspase-9 mRNA and cleaved caspase-9 protein in rats with myocardial I/R. However, pretreatment with LY294002 significantly reduced the cardioprotective effects of IGF-1. Conclusion Treatment with IGF-1 may confer cardiac protection against in vivo myocardial I/R injury via the PI3K/Akt pathway in rats. |
Databáze: | Directory of Open Access Journals |
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