Abstract
Purpose: To determine the protective effect of ginkgolide B (GB) against isoproterenol (ISO)-induced chronic heart failure in a rat model.
 Methods: A total of 32 male Wistar rats were randomly divided into 4 groups. Rats in control group received only saline, while rats in GB alone group were injected with GB at a dose of 20 mg/kg body weight (bwt) intraperitoneally (i.p). Another group of rats was injected with ISO subcutaneously (s.c.) at a dose of 85 mg/kg for 2 days (ISO group). Rats in the GB+ISO group were administered GB at a dose of 20 mg/kg, i.p., for 7 days prior to exposure to ISO s.c. at a dose of 85 mg/kg.
 Results: Rats pre-treated with GB for 7 days prior to ISO exposure showed a significant decrease in cardiac infarct size, and marked decreases in the levels of cardiac biomarkers, inflammatory and apoptotic biomarkers, and lipid peroxidation (p < 0.05), but significant improvement in the levels ofendogenous antioxidants (p < 0.05). In addition, GB administration resulted in marked increases in the protein expression levels of heme oxygenase-1 (HO-1) and Nrf2 in cardiac tissue (p < 0.05).
 Conclusion: These results indicate that pre-treatment of chronic heart failure rats with GB for 7 consecutive days considerably lowered inflammatory and apoptotic markers via upregulation of Nrf2/HO-1 signaling pathway. Thus, GB has cardioprotective potential in humans.
 Keywords: Ginkgolide B, Nrf2/HO-1, Inflammatory markers, Apoptotic markers, Antioxidants
Highlights
Myocardial infarction (MI) or heart attack (HA) is one of the most predominant and deadly forms of ischemic heart disease (IHD), based on the fact that it claims more lives than any other cardiovascular disease (CVD)
The major apoptotic markers i.e. caspase-3 and caspase-9 were assayed in cardiac tissue homogenate using a commercial assay kit from Abcam (Cambridge, UK) based on manufacturer's instructions
The results obtained in this animal study have highlighted the cardioprotective potential of Ginkgolide B (GB) through significant decreases in cardiac infarct size and reduced levels of cardiac markers, inflammatory biomarkers and biomarkers of apoptosis
Summary
Myocardial infarction (MI) or heart attack (HA) is one of the most predominant and deadly forms of ischemic heart disease (IHD), based on the fact that it claims more lives than any other cardiovascular disease (CVD). The National Center for Cardiovascular Diseases in China reported that the number of CVD patients MI patients, is continuously on the increase. The cost of treating MI reached 2.3 billion US dollars in 2015, an indication of the indirect and considerable economic burden of the disease on China [3,4]. Myocardial infarction is caused by lack of sufficient blood supply to the heart muscles, leading to necrosis or apoptosis of the myocardium (heart muscle). This is accompanied by numerous pathophysiological and biochemical changes including hypoxia, hyperlipidemia, oxidative stress, and inflammatory responses [5,6]. Many researchers have focused on natural antioxidant and anti-inflammatory agents for treating or managing MI-related conditions [7,8]
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