RESUMO
Objective: Myocardial infarction (MI) is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles. Beta-blockers and calcium antagonists are just two of the common medications used to treat MI. However, these have reportedly been shown to be either ineffective or to have undesirable side effects. Extract of Ginkgo biloba leaves (GBE), a Chinese herbal product offers special compatibility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress. In order to better understand how GBE affects MI in rats insulted by isoprenaline (ISO), the current study was designed. Methods: The heart weight index, serum lipid profile, cardiac marker enzymes, endogenous antioxidants [catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), nitrites and malondialdehyde (MDA)], inflammatory mediators [tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6)], immunohistochemical expressions of B-cell lymphoma factor-2 (Bcl-2), extracellular signal-regulated kinase (ERK1/2), and mammalian target of rapamycin (mTOR) and histopathological analysis were used to assess the cardioprotective properties of GBE. Results: The findings showed that GBE effectively attenuated myocardial infarction by boosting the body's natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes. The expression of Bcl-2, ERK1/2 and mTOR was increased while the histomorphological alterations were reversed. Conclusion: The cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na+, K+-ATPase activity.
RESUMO
This study investigated the modulatory effect of Ginkgo biloba extract on lead acetate-induced endothelial dysfunction. Animals were administered GBE (50 mg/kg and 100 mg/kg orally) after exposures to lead acetate (25 mg/kg orally) for 14 days. Aorta was harvested after euthanasia, the tissue was homogenised, and supernatants were decanted after centrifuging. Oxidative, nitrergic, inflammatory, and anti-apoptotic markers were assayed using standard biochemical procedure, ELISA, and immunohistochemistry, respectively. GBE reduced lead-induced oxidative stress by increasing SOD, GSH, and CAT as well as reducing MDA levels in endothelium. Pro-inflammatory cytokines (TNF-α and IL-6) were reduced while increasing Bcl-2 protein expression. GBE lowered endothelin-I and raised nitrite levels. Histological changes caused by lead acetate were normalised by GBE. Our findings suggest that Ginkgo biloba extract restored endothelin-I and nitric oxide functions by increasing Bcl-2 protein expression and reducing oxido-inflammatory stress in endothelium.
