Vinpocetine attenuates myocardial ischemia/reperfusion injury in mice by suppressing oxidative stress, inflammation, and apoptosis.

Myocardial ischemia-reperfusion injury (MIRI) represents a frequent and serious complication that arises after acute myocardial infarction. During MIRI, the NLRP3 inflammasome exerts a critical function in controlling inflammatory processes. Vinpocetine (VIN) is mainly used as a neuroprotective agent in cerebrovascular diseases, and it exhibits both antioxidant properties and anti-inflammatory activities. Earlier investigations indicated that VIN can suppress NLRP3 inflammasome activation. Nevertheless, its specific contribution to cardiac MIRI and the mechanisms involved have yet to be fully unraveled. The current study sought to examine the cardioprotective actions of VIN in a murine MIRI model and to determine whether the protection is linked to the NLRP3 inflammasome pathway. MIRI was induced in mice through ischemia/reperfusion (I/R) procedures. Cardiac performance and the extent of myocardial damage were assessed via echocardiography, determination of infarct area, measurement of serum cardiac enzymes, evaluation of oxidative stress markers, and analysis of apoptosis-associated protein levels. Findings demonstrated that pretreatment with VIN at a dose of 10 mg/kg substantially ameliorated I/R-triggered impairment of cardiac function, diminished infarct size, lowered circulating creatine kinase (CK) together with lactate dehydrogenase (LDH) concentrations, and potently attenuated oxidative stress as well as cardiomyocyte apoptosis. Moreover, I/R strongly triggered NLRP3 inflammasome assembly and elevated concentrations of its downstream inflammatory factors, while VIN pretreatment effectively prevented these alterations. Further experiments using MCC950, a selective NLRP3 inflammasome inhibitor, showed that MCC950 exerted cardioprotective effects comparable to those of VIN, and co-administration of MCC950 and VIN did not confer additional significant benefits. Observations in the current work imply that heart-protective benefits conferred by VIN occur to a substantial degree via blockade of NLRP3 inflammasome activity. Taken together, pretreatment with VIN reduces the severity of MIRI in the murine model through attenuation of oxidative damage, cellular apoptosis, and inflammation-related cascades, in which suppression of the NLRP3 inflammasome may constitute one key pathway accounting for such beneficial outcomes.