2 activities by antioxidant mechanisms confer cardioprotection on Ginkgo biloba supplement against isoprenaline-induced myocardial infarction in rats (original) (raw)

Pharmacological Research - Modern Chinese Medicine

Abstract

Background: Myocyte necrosis and apoptosis can be severely induced by acute adrenergic stimulation due to the activation of several cell signalling pathways. However, uncertainty exists regarding the potential cardioprotective effects of Ginkgo biloba (GBS), a Chinese herbal supplement rich with antioxidants, on isoprenaline (ISO)-induced myocardial infarction. Therefore, this work was designed to investigate the cardioprotective mechanisms of GBS on ISO-induced myocardial infarction. Methods: Animals were selected into four groups. Groups 1 and 2 were pre-treated with normal saline (10 mL/kg i.p) for 28 days. Groups 3 and 4 received GBS (50 mg/kg, i.p) for 28 days. However, groups 2 and 4 were administered ISO (150 mg/kg, s.c) on days 27 and 28 respectively. Following the end of 28-day experiment, animals were euthanised and serum as well as heart tissue were harvested and processed for biochemical and histological examinations. Results: Our results showed that ISO induced cardiac necrosis, evidenced by increased levels of cardiac injury enzymes (LDH, GGT, CK-MB and cT-1), oxidative stress markers such as GSH, SOD, and CAT levels were significantly reduced while MDA and nitrite concntration were significantly increased. Inflammatory cytokines (IL-6 and TNF-α) were significantly increased while decreasing Bcl-2, mTOR and ERK 1/2 cardiac immunoexpressions. Moreso, histological investigation revealed degeneration of cardiomyofibres together with patchy necrosis. However, pre-treatment with GBS significantly inhibited apoptotic processes evidenced by increased antioxidant-mediated activation of Bcl-2, mTOR and ERK 1/2. GBS also suppressed the release of cardiac injury enzymes and histological changes were significantly improved. Conclusion: GBS protects myocardium against ISO-induced infarction by mechanisms related to antioxidantmediated by enhancement of Bcl-2/mTOR/ERK 1/2 activities.

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