Original Article
Protective effects of PI3KCG gene on acute myocardial infarction
Abstract
Background: To study the protective effects of recombinant phosphatidylinositol 3-kinase p110 gamma (rPLV-PI3KCG) lentiviral vector in Sprague-Dawley (SD) rats with acute myocardial infarction (AMI).
Method: The AMI rat models were established by ligaturing left anterior descending coronary artery. The rPLV-PI3KCG or empty lentiviral vectors were injected at the edge of the infarct zone. The experiment was divided randomly into four groups (n=8): (I) Sham group; (II) AMI group; (III) AMI + empty vector injection group (AMI + E group); and (IV) AMI + PLV-PI3KCG injection group (AMI + PLV-PI3KCG group). The ultrasonic cardiogram (UCG) was used to compare the structural or functional changes among the four groups after operation for 10 days. Meanwhile, the rats were sacrificed and HE staining was used to compare the myocardial tissue changes among the four groups. The immunofluorescence and western blots were performed to compare the angiogenesis in the infarct region and explore the mechanism of the protective effects of PI3KCG gene on AMI rats.
Results: Compared with AMI group and AMI + E group, in the AMI + PLV-PI3KCG group, left ventricular end diastolic diameter (LVEDd) was decreased, left ventricular ejection fraction (LVEF%) was significantly increased, and vascular endothelial growth factor (VEGF) expression was significantly increased in the infarct region (P<0.05); PI3KCG, pAkt/Akt, HIF-1a, and Bcl-2/Bax protein expressions were significantly increased (P<0.05).
Conclusions: The rPLV-PI3KCG injection could improve the cardiac function, relieve the cardiac injury after the AMI operation. PI3KCG gene could play the protection role in the AMI process possibly by activating PI3K/Akt signal pathway, inhibiting apoptosis and promoting angiogenesis.
Method: The AMI rat models were established by ligaturing left anterior descending coronary artery. The rPLV-PI3KCG or empty lentiviral vectors were injected at the edge of the infarct zone. The experiment was divided randomly into four groups (n=8): (I) Sham group; (II) AMI group; (III) AMI + empty vector injection group (AMI + E group); and (IV) AMI + PLV-PI3KCG injection group (AMI + PLV-PI3KCG group). The ultrasonic cardiogram (UCG) was used to compare the structural or functional changes among the four groups after operation for 10 days. Meanwhile, the rats were sacrificed and HE staining was used to compare the myocardial tissue changes among the four groups. The immunofluorescence and western blots were performed to compare the angiogenesis in the infarct region and explore the mechanism of the protective effects of PI3KCG gene on AMI rats.
Results: Compared with AMI group and AMI + E group, in the AMI + PLV-PI3KCG group, left ventricular end diastolic diameter (LVEDd) was decreased, left ventricular ejection fraction (LVEF%) was significantly increased, and vascular endothelial growth factor (VEGF) expression was significantly increased in the infarct region (P<0.05); PI3KCG, pAkt/Akt, HIF-1a, and Bcl-2/Bax protein expressions were significantly increased (P<0.05).
Conclusions: The rPLV-PI3KCG injection could improve the cardiac function, relieve the cardiac injury after the AMI operation. PI3KCG gene could play the protection role in the AMI process possibly by activating PI3K/Akt signal pathway, inhibiting apoptosis and promoting angiogenesis.
