Key result
Ranolazine administration attenuated the severity of isoprenaline-induced myocardial injury in both nondiabetic and diabetic rats by modulating AMPK expression and inhibiting apoptosis.
Why the study?
Diabetes increases myocardial sensitivity to ischemic injury and impairs cardioprotective responses, prompting evaluation of the cardioprotective effects and AMPK-modulating role of ranolazine during myocardial infarction.
Does ranolazine reduce myocardial injury in nondiabetic and diabetic male rats subjected to isoprenaline-induced acute myocardial infarction?
Does ranolazine reduce myocardial injury in nondiabetic and diabetic male rats subjected to isoprenaline-induced acute myocardial infarction?
Ranolazine demonstrates cardioprotective effects against acute myocardial infarction in both diabetic and nondiabetic rat models by modulating AMPK and inhibiting apoptosis.
Does not support clinical use in MI yet; extends AMPK-apoptosis evidence to diabetic and nondiabetic rat models.
Diabetes increases the sensitivity of myocardium to ischemic damage and impairs response of the myocardium to cardioprotective interventions. The present study aimed to elucidate the potential cardioprotective effect provided by ranolazine during myocardial infarction in nondiabetic and diabetic male rats. As AMP-activated protein kinase (AMPK) has been shown to be involved in the cellular response to ischemic injury, in this context, the present animal study evaluated the modulating role of ranolazine in the AMPK expression in isoprenaline-induced myocardial ischemic rat model. Male rats were divided into 2 experiments: experiment I and II (nondiabetic and diabetic rats) and assigned to normal control, saline control for isoprenaline, isoprenaline control, and ranolazine-treated groups. Ranolazine administration revealed effectiveness in attenuating the severity of isoprenaline-induced myocardial injury in both nondiabetic and diabetic rats as revealed by ECG signs, histopathological score, and apoptotic markers via abrogating the increments in the inflammatory and oxidative stress markers and modulating AMPK expression. Therefore, the current cardioprotective effect of ranolazine was, at least in part, mediated through inhibition of apoptosis and modulation of AMPK expression, encouraging considering the utility of ranolazine in protection from acute myocardial infarction.
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Tawfik et al. (2019) studied Isoprenaline-induced acute myocardial infarction. Ranolazine vs. Normal control, saline control, and isoprenaline control was evaluated on Severity of isoprenaline-induced myocardial injury (ECG signs, histopathological score, apoptotic markers, inflammatory and oxidative stress markers, AMPK expression). Ranolazine administration attenuated the severity of isoprenaline-induced myocardial injury in both nondiabetic and diabetic rats by modulating AMPK expression and inhibiting apoptosis.
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