Background: Myocardial infarction (MI) is a leading cause of morbidity and mortality. It is associated with oxidative stress, apoptosis and inflammation. Zinc (Zn) and vitamin E (VE) are known to exert antioxidant and anti-inflammatory effects.
Aim of the Work: Evaluate the cardioprotective potential of Zn, VE and their combination against isoprenaline (ISO)-induced myocardial infarction in adult male albino rats.
Materials and Methods: Forty rats divided into five groups; I (control), II (ISO group): rats were injected subcutaneously (SC) with ISO (100 mg/kg) on the 20th and 21st days at interval of 24 h. Groups III (Zn group), IV (VE group) and V (ZE group): rats received respectively daily Zn (30 mg/kg), VE (100 mg/kg) or combination of both orally for 21 days and injected with ISO as group II. On the 22nd day, electrocardiography, biochemical and histological studies were done. Myocardial sections were subjected to H&E, caspase-3 and beclin 1 immunohistochemical stains. This was followed by morphometric and statistical analysis.
Results: Group II exhibited significant electrocardiographic and biochemical changes compared to the control; deterioration of cardiac function with elevated cardiac enzymes, MDA, TNF-α and mTOR, in addition to reduced SOD, IL-10 and AMPK. Myocardial sections showed disturbed architecture with marked inflammatory infiltration and significantly increased caspase-3 and decreased beclin 1 immunoexpression. Groups III and IV revealed decreased cardiac enzymes, MDA, TNF-α and mTOR, in addition to elevated SOD, IL-10 and AMPK. Myocardial sections showed nearly normal histology with significantly decreased caspase-3 and increased beclin 1 immunoexpression. Group V presented the most protection with results significant to both groups III and IV.
Conclusion: Combined Zn and VE pretreatment proved to have protective effect against ISO-induced MI more than using either of them alone regarding the electrocardiography, biochemical and histological parameters and this was through targeting autophagy and modulating its AMPK-mTOR pathway