Background: Myocardial infarction (MI), a critical condition of ischemic heart disease, significantly contributes to global morbidity and mortality rates. L-carnitine, an essential metabolic cofactor, holds therapeutic promise in management of MI, although its precise mechanisms remain unclear. Objective: This research aimed to explore the cardioprotective potential of L-carnitine in male rats subjected to MI, with a particular focus on potential role of Nrf2/Parkin signaling pathway. Materials and Methods: Rats were divided into four groups, each comprising eight animals (n=8): a control group, an L-carnitine group (receiving 100 mg/kg/day orally for 14 days), an ISO group (MI induced by subcutaneous administration of 85 mg/kg isoprenaline on days 13 and 14), and an L-carnitine + ISO group (treated with L-carnitine 100 mg/kg/day orally for 2 weeks, followed by ISO administration). Results: Isoprenaline induced MI, as indicated by significant ECG changes, elevated cardiac biomarkers, histopathological damage, and reduced desmin expression in immunohistochemistry. Moreover, there was an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa B (NF-κB), along with enhanced caspase-3 immunohistochemical staining. These alterations were paralleled by a reduction in total antioxidant capacity (TAC), Parkin levels, and Nrf2 immunohistochemical staining. L-carnitine treatment attenuated these adverse effects. Conclusion: L-carnitine exerts cardioprotective effects, which may be attributed to its anti-inflammatory, antioxidant, and anti-apoptotic properties, in addition to promoting mitophagy through upregulation of Parkin via Nrf2 signaling pathway |
