Key result
Rosuvastatin postconditioning decreased myocardial infarct size compared to ischemia-reperfusion alone in a rat model.
Why the study?
Does postconditioning with rosuvastatin reduce myocardial ischemia-reperfusion injury in rats?
Does postconditioning with rosuvastatin reduce myocardial ischemia-reperfusion injury in rats?
Rosuvastatin postconditioning reduces myocardial ischemia-reperfusion injury in a rat model, potentially through the inhibition of HMGB1 expression.
Answers are grounded in this paper and cite their sources.
Rosuvastatin postconditioning may protect against experimental ischemia-reperfusion injury; leaves open translation to clinical cardioprotection.
High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia-reperfusion (I/R) injury. Rosuvastatin (RS) preconditioning has been reported to reduce myocardial I/R injury. The aim of this study was to investigate whether postconditioning with RS is able to reduce myocardial I/R injury by inhibiting HMGB1 expression in rats. Anesthetized male rats were subjected to ischemia for 30 min and treated once with RS (10 mg/kg, i.v.) 5 min prior to reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that RS postconditioning significantly decreased the infarct size and the activities of LDH and CK following 4 h reperfusion (all P<0.05). RS postconditioning also significantly inhibited the increase of MDA levels and the reduction of SOD activity (both P<0.05). RS postconditioning was able to significantly inhibit the HMGB1 expression induced by I/R. The present study suggested that postconditioning with RS reduces myocardial I/R injury, which may be associated with the inhibition of HMGB1 expression.
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Du et al. (2013) studied Myocardial ischemia-reperfusion injury (n=40). Rosuvastatin vs. Ischemia and reperfusion (I/R) without rosuvastatin was evaluated on Infarct size (percentage of risk area volume) (p=<0.05). Rosuvastatin postconditioning decreased myocardial infarct size compared to ischemia-reperfusion alone in a rat model.
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