Why the study?
The study was conducted to evaluate the role of preconditioning co-treatment with rosuvastatin and dapagliflozin in myocardial ischemia/reperfusion injury and to investigate the underlying mechanism.
Does co-treatment with rosuvastatin and dapagliflozin improve cardioprotection against myocardial ischemia/reperfusion injury in rats compared to either drug alone?
Does co-treatment with rosuvastatin and dapagliflozin improve cardioprotection against myocardial ischemia/reperfusion injury in rats compared to either drug alone?
Co-treatment with rosuvastatin and dapagliflozin synergistically protects against myocardial ischemia/reperfusion injury in rats by activating the PI3K/Akt/mTOR signaling pathway.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rat I/R model; leaves open whether RSV-DGZ co-treatment confers clinical cardioprotection.
Objective The purpose of the present study was to evaluate the role of co-treatment of rosuvastatin (RSV) and dapagliflozin (DGZ) preconditioning in myocardium ischemia/reperfusion (I/R) injury and to further investigate the underlying mechanism. Methods Sprague-Dawley (SD) rats ( n = 25) were divided into five groups randomly: (1) Sham, (2) I/R, (3) I/R + RSV (10 mg/kg), (4) IR + DGZ (1 mg/kg), and (5) I/R + RSV (10 mg/kg) + DGZ (1 mg/kg). The I/R model was induced with 30 min of left anterior descending occlusion followed by 120 min of reperfusion. Results In vivo pretreatment with RSV and DGZ, respectively, showed a significant reduction of infarction size, a significant increase in the levels of left ventricular systolic pressure, and maximal rate increase in left ventricular pressure (+d p /d t max ), decrease in the levels of left ventricular end-diastolic pressure (LVEDP), maximal rate of decrease of left ventricular pressure (−d p /d t max ) and activity of cardiac enzymes of creatine kinase (CK), creatine kinase MB isoenzymes (CK-MB), and hyper-tensive cardiac troponin I compared with the I/R group. H9C2 cells were exposed to hypoxia/reoxygenation to simulate an I/R model. In vitro administration of 25 µM RSV and 50 µM DGZ significantly enhanced cell viability, upregulated the expression levels of p-PI3K, p-Akt, p-mTOR, and Bcl-2, whereas it downregulated cleaved-caspase3, Bax. TUNEL assay indicated that pretreatment with RSV and DGZ decreased the apoptosis of H9C2 cells. Conclusion The combination of RSV and DGZ significantly enhances the cardioprotective effects compared with RSV or DGZ alone. RSV and DGZ have the potential cardioprotective effects against I/R injury by activating the PI3K/AKt/mTOR signaling pathway.
No takes yet. Share an insight, caveat, or question.
Gong et al. (2020) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: