Coconut kernel protein in diet protects the heart by beneficially modulating endothelial nitric oxide synthase, tumor necrosis factor-alpha, and nuclear factor-kappaB expressions in experimental myocardial infarction

Coconut kernel protein in diet protects the heart by beneficially modulating endothelial nitric oxide synthase, tumor necrosis factor-alpha, and nuclear factor-kappaB expressions in experimental myocardial infarction

Previous studies conducted in our laboratory revealed that coconut kernel protein has a significant cardioprotective effect on isoproterenol-induced myocardial infarction in rats. In the present study, we explored the possible protective mechanism of coconut kernel protein during acute myocardial infarction. Coconut kernel protein (50 mg/100 g) was administered to Sprague-Dawley rats orally for 45 days. Isoproterenol (20 mg/100 g) was injected subcutaneously at an interval of 24 hours twice to induce myocardial infarction. Myocardial infarction was confirmed by the abnormal activities of cardiac marker enzymes in serum. Activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase were decreased ( p < 0.05) in the heart of isoproterenol-treated rats, whereas pretreatment with coconut kernel protein increased ( p < 0.05) these activities. An improved antioxidant status in these rats was further confirmed by the increased level of reduced glutathione and decreased level of lipid peroxidation products. Nitric oxide synthase (NOS) activity in the heart and nitrite level in blood were increased ( p < 0.05) in coconut kernel protein-treated rats administered with isoproterenol compared to isoproterenol control rats. Coconut protein pretreatment upregulated the expression of endothelial nitric oxide synthase (eNOS), whereas expressions of nuclear factor-kappaB (NF-kB) and tumor necrosis factor-alpha (TNF-a) were downregulated in isoproterenol-treated rats. These findings suggest that the protective effects of coconut kernel protein may be mediated in part through upregulation of nitric oxide production, antioxidant mechanisms, and its ability to inhibit TNF-a and NF-kB activation.