Key result
Shen-fu injection preconditioning significantly decreased myocardial infarct size and apoptosis in diabetic rats subjected to ischemia-reperfusion injury via a PI3K/Akt-dependent pathway.
Why the study?
Does Shen-fu injection preconditioning reduce myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats?
Does Shen-fu injection preconditioning reduce myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats?
Shen-fu injection preconditioning protects diabetic rat hearts from ischemia-reperfusion injury via the PI3K/Akt-dependent pathway.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in diabetic rat models; human trials required before any clinical consideration.
The aim of this paper is to investigate whether Shen-fu injection (SFI), a traditional Chinese medicine, could attenuate myocardial ischemia-reperfusion (MI/R) injury in diabetes. Streptozotocin-induced diabetic rats were randomly assigned to the Sham, I/R, SFI preconditioning, and SFI plus wortmannin (a phosphatidylinositol 3-kinase inhibitor) groups. After the treatment, hearts were subjected to 30 min of coronary artery occlusion and 2 h reperfusion except the Sham group. Myocardial infarct size and cardiomyocytes apoptosis were increased significantly in MI/R group as compared with the Sham group. SFI preconditioning significantly decreased infarct size, apoptosis, caspase-3 protein expression, MDA level in myocardial tissues, and plasma level of CK and LDH but increased p-Akt, p-eNOS, bcl-2 protein expression, and SOD activity compared to I/R group. Moreover, SFI-induced cardioprotection was abolished by wortmannin. We conclude that SFI preconditioning protects diabetic hearts from I/R injury via PI3K/Akt-dependent pathway.
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Wu et al. (2010) studied Myocardial ischemia-reperfusion injury in diabetes. Shen-fu injection (SFI) preconditioning vs. Ischemia/Reperfusion (I/R) without SFI was evaluated on Myocardial infarct size and cardiomyocytes apoptosis. Shen-fu injection preconditioning significantly decreased myocardial infarct size and apoptosis in diabetic rats subjected to ischemia-reperfusion injury via a PI3K/Akt-dependent pathway.
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