Key result
IGF-1 reduces infarct size and apoptosis in rat myocardial I/R injury via PI3K/Akt signaling.
Why the study?
It remained unknown whether insulin-like growth factor-1 (IGF-1) could attenuate myocardial ischemia/reperfusion injury in vivo by activating the PI3K/Akt pathway.
Does IGF-1 reduce myocardial ischemia/reperfusion injury in a rat model?
Does IGF-1 reduce myocardial ischemia/reperfusion injury in a rat model?
IGF-1 protects against myocardial ischemia/reperfusion injury in rats by activating the PI3K/Akt pathway.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for IGF-1 cardioprotection in ischemia/reperfusion; human trials needed before clinical consideration.
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.
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Liao et al. (2019) studied Myocardial ischemia/reperfusion injury. Insulin-like growth factor-1 (IGF-1) vs. Myocardial I/R without IGF-1 or with LY294002 pretreatment was evaluated on Myocardial infarct size, myocardial cell apoptosis, and serum biomarkers (LDH, CK-MB, cTnI). IGF-1 treatment decreased myocardial infarct size, apoptosis, and cardiac biomarkers in rats with myocardial ischemia/reperfusion injury, an effect reduced by PI3K/Akt inhibition.
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