Abstract
Ginkgolide B (GB) is an extract of dried Ginkgo biloba leaves and possesses various pharmacological activities in the cardiovascular system. Herein, we aim to assess the available preclinical evidence and possible mechanisms of GB for myocardial ischemia/reperfusion injury. The study quality score was assessed using the CAMARADES 10-item checklist. Rev-Man 5.3 software was used for data analyses. Nineteen studies with total 437 animals were included for analysis. Meta-analyses indicated that GB interventions significantly reduce myocardial infarct size and cardiac markers when compared with control (P < 0.05). The possible mechanisms via which GB exerts cardioprotective effects are mainly associated with anti-oxidation, anti-inflammation, anti-apoptosis, and improvement of energy metabolism. Our study indicates that GB might be a promising cardioprotective agent for myocardial ischemia/reperfusion injury and may contribute to future clinical trial design.
Highlights
Coronary heart disease (CHD) is the leading cause of death and disability globally (Ibanez et al, 2015)
The present study demonstrated that GB could alleviate the myocardial I/R injury, mainly through the antioxidation, anti-inflammation, anti-apoptosis, and the improvement of energy metabolism
The present study showed that GB could increase the level of antioxidant enzymes such as SOD, GSHPx and CAT, maintain the dynamic balance of oxygen free radicals formation, restrain trigger of lipid peroxidation, protect biomembranes’ integrity and function, and decrease the release of MDA from mitochondria, thereby exerts cardioprotective effect in through antioxidation
Summary
Coronary heart disease (CHD) is the leading cause of death and disability globally (Ibanez et al, 2015). Acute myocardial infarction (AMI) is one critical clinical presentation of coronary artery disease (Yellon and Hausenloy, 2007). Restoration of blood flow through thrombolysis or primary percutaneous coronary intervention has been proved to be the most effective method to rescue ischemic myocardium, reduce infarct size, and improve the clinical outcomes (Frank et al, 2012). Over the past 3 decades, numerous therapeutic strategies, both pharmacologic and non-pharmacologic, have been proposed to ameliorate the myocardial I/R injury in animal experiments. It is worthy to find a novel cardioprotective therapeutic intervention to prevent further tissue injury caused by reperfusion
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