Abstract
Elderly people are more likely to experience myocardial infarction (MI) than young people, with worse post-MI mortality and prognosis. Ginkgo biloba extract 50 (GBE50) is an oral GBE product that matches the German product, EGb761, which has been used to treat acute myocardial infarction (AMI). The extraction purity of GBE50 was improved to form a new formulation, Ginkgo biloba extract 80 (GBE80). This study investigates the effect of GBE80 on aged acute myocardial infarction rats. GBE80 injection is a novel formulation that was prepared by mixing Ginkgo flavonoids and lactones in a 4:1 weight ratio, with a Ginkgo content of more than 80%. Cell Counting Kit-8 was used to determine the biological safety and protective effect of GBE80 on cardiomyocytes against oxidative damage. An aged AMI rat model was developed and used to determine the myocardial infarction weight ratio using triphenyltetrazolium chloride staining. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) was applied to detect cell apoptosis in myocardial tissue. Western blotting and immunohistochemistry were used to measure the protein levels of members of the AKT/GSK3β/β-catenin pathway in vitro and in vivo, respectively. We found that GBE80 in vitro suppressed H2O2-induced cytotoxicity by promoting AKT/GSK3β/β-catenin signaling, while it did not show cytotoxicity to normal cardiomyocytes in the 0–500 μg/ml dose range. After 7 days of administration to aged AMI rats, GBE80 markedly reduced the weight ratio of the infarction and inhibited cell apoptosis in myocardial tissue. Furthermore, the AKT/GSK3β/β-catenin signaling pathway was activated by GBE80. These results suggest that GBE80 injection effectively inhibited AMI-induced myocardial damage and in vitro H2O2-induced cardiomyocyte cytotoxicity by activating the AKT/GSK3β/β-catenin signaling pathway.
Highlights
Myocardial infarction (MI) is a common clinical adverse cardiovascular event, which can endanger the lives of patients
Ginkgo biloba extract 80 (GBE80) significantly increased pAKT, pGSK3β, and β-catenin proteins levels in a dosedependent manner. These results revealed that GBE80 activated the AKT/glycogen synthase kinase 3β (GSK3β)/β-catenin signaling pathway, and played an antioxidant role in cardiomyocytes in vitro
The present study aimed to investigate the protective effects of GBE80 injection on acute myocardial ischemia injury and its possible regulatory mechanisms in vivo and in vitro
Summary
Myocardial infarction (MI) is a common clinical adverse cardiovascular event, which can endanger the lives of patients. The Framingham Heart Study indicated that higher age is significantly associated with risk of myocardial infarction (Ngwa et al, 2021). Compared with middle-aged men (55–64 years), the MI incidence of elderly men (85–94 years) was more than two times higher, and increased by more than five times for women (women aged 55–64 years vs 85–94 years) (National Heart, Lung, and Blood Institute, 2006; Qipshidze Kelm et al, 2018). The GISSI-2 (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-2) study showed that the risk of cardiac rupture increases significantly with age in patients receiving thrombolytic therapy for reperfusion after a first MI. The proportion of the global population aged over 60 will increase from 10.0% in 2000 to 21.8% in 2050 and 32.2% in 2,100 (Lutz et al, 2008). These predictions have prompted researchers to seek more effective treatments for MI
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