Improvement in Cardiac Troponins and Proinflammatory Cytokines Following Dacryodes Edulis Compounds Treatment in Ketamine-Induced Myocardial Injury in Wistar Rats
Keywords:
Dacryodes edulis, Ketamine-induced myocardial injury, Cardiac troponins, Pro-inflammatory cytokines, Cardioprotection, Phytochemicals.Abstract
Aim: To evaluate the cardioprotective effects of Dacryodes edulis compounds on ketamine-induced myocardial injury in Wistar rats by assessing serum troponins and pro-inflammatory cytokines.
Research Design: Experimental, randomized controlled animal study.
Place and Duration: Conducted at the Department of Human Anatomy, Nile University of Nigeria, Abuja, Nigeria, over a period of three months in 2024.
Methodology: Forty-eight male Wistar rats were randomly assigned to eight groups and administered ketamine at doses of 100, 150, and 200 mg/kg to induce myocardial injury. Treatment groups received concomitant oral doses of Dacryodes edulis methanolic extract and its fractions (saponins, alkaloids, flavonoids). Serum levels of cardiac troponins T and I, IL-6, and TNF-α were measured using ELISA kits after 21 days of treatment. Phytochemical analysis of the plant fractions was performed to identify bioactive compounds. Data were analyzed statistically, with p < 0.05 considered indicative of significant differences between groups.
Results: Ketamine significantly elevated serum troponins and pro-inflammatory cytokines compared to controls. Treatment with Dacryodes edulis extracts, especially the methanolic and flavonoid-rich fractions, markedly reduced troponin and cytokine levels, approaching those of the control group. Phytochemical analysis revealed high concentrations of flavonoids, saponins, and alkaloids, correlating with observed cardioprotective effects.
Conclusion: Dacryodes edulis compounds exhibit significant cardioprotective effects against ketamine-induced myocardial injury in rats, primarily through their antioxidant and anti-inflammatory properties. These findings suggest its potential as a natural therapeutic agent for mitigating drug-induced cardiac damage, warranting further investigation.

