Baicalein pretreatment confers cardioprotection against acute myocardial infarction by activating the endothelial nitric oxide synthase signaling pathway and inhibiting oxidative stress.

Baicalein, a flavonoid purified from the root of Scutellaria baicalensis Georgi, is well known for its anti-inflammatory and anti-oxidative properties. The present study aimed to evaluate the cardioprotective effect of baicalein in a rat model of acute myocardial infarction and investigate the potential molecular mechanisms of this effect. The acute myocardial infarction model was prepared by permanently occluding the left anterior descending artery. Baicalein and/or the endothelial nitric oxide synthase (eNOS) inhibitor L-NAME was injected prior to the induction of acute myocardial infarction. In the vehicle-treated group, acute myocardial infarction resulted in a markedly increased infarction size and elevated levels of plasma cardiac enzymes, including creatine kinase, the MB isoenzyme of creatine kinase, lactate dehydrogenase and cardiac troponin T, compared with those in the sham-surgery group. In the baicalein treatment group, the infarcted area and plasma levels of the cardiac enzymes were significantly decreased compared with those in the vehicle-treated group. In addition, pretreatment with baicalein potently increased the levels of eNOS protein and nitric oxide production in the infarcted rats. Furthermore, myocardial oxidative stress was attenuated by baicalein preconditioning following acute myocardial infarction. However, L-NAME inihibted the cardioprotective effects of baicalein. These data indicate that baicalein protects against acute myocardial infarction-induced injury by activating eNOS signaling and inhibiting oxidative stress.