In the present study, rat hearts were isolated and perfused using the Langendorff technique to establish a high-throughput and potentially reliable I/R model. The Langendorff mouse heart model is widely used in studies of myocardial function and responses to injury ( 17). Therefore, further studies investigating the mechanisms of protection are required. In addition, there has been no clear histological or immunohistochemical evidence showing the cardioprotective effect of BA to date. However, the cardioprotective properties have not been confirmed and the mechanism has not been fully characterized. Studies have demonstrated that BA can suppress the proliferation of vascular smooth muscle cells ( 9) and exert cardioprotective effects against hypoxia/reoxygenation injury ( 12– 16). Baicalin (BA C 21H 18O 11, 7-glucuronic acid, 5,6-dihydroxy-flacone), a Chinese traditional medicinal herb, possesses antioxidant properties and free radical scavenging activity ( 8– 12). However, the effective ingredients in the majority of these medications have not been identified. Thus, protection against I/R injury in the heart is of marked importance.Ĭhinese herbal medicine has been used to treat diseases for thousands of years and it has recently attracted the attention of practitioners of Western medicine. Numerous studies have indicated that cell apoptosis is associated with a variety of damaging stimuli, particularly continuous I/R, in vitro and in the intact heart in vivo( 3– 7). Following cell I/R, apoptosis is one of the major pathways that leads to the process of cell death. I/R injury of the heart is the underlying pathophysiology of acute myocardial infarction (AMI), which is one of the most common causes of mortality globally ( 2). Ischemia-reperfusion (I/R) injury remains the leading cause of morbidity and mortality in all developed countries and is a large economic burden in the treatment and care of patients ( 1). To the best of our knowledge, this study is the first evaluation of the efficacy of BA in isolated rat hearts using histology and immunohistochemistry, providing a foundation for the use of BA in the treatment of acute myocardial infarction. In conclusion, these results demonstrated that BA exerts a dose-dependent protective effect on I/R injury in isolated rat hearts, the mechanisms of which may be associated with antioxidant and anti-apoptosis properties. The FCM results indicated that apoptosis was significantly lower in the BA groups than in group II (P<0.05) and that the protective effect was dose-dependent. Furthermore, histology and immunohistochemistry results showed that the infarct size was reduced and vessel density was augmented in the BA groups (P<0.01) compared with group II. Compared with group II, the BA groups demonstrated improved left ventricular function, reduced CK and LDH release in the coronary effluent and increased SOD and MDA activity (P<0.05). The apoptotic cardiomyocytes were determined using flow cytometry (FCM). Myocardial infarct size and vascular density were assessed using histology and immunohistochemistry. The degree of heart injury caused by the I/R was assessed by evaluating left ventricular function and by detecting the levels of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary effluent and the myocardial superoxide dismutase (SOD) and malondialdehyde (MDA) levels in the isolated rat hearts. All animals (n=50) were randomly divided into five groups (n=10 in each): I, normal control II, I/R III, I/R plus 20 mg/kg BA IV, I/R plus 40 mg/kg BA and V, I/R plus 80 mg/kg BA. Sprague-Dawley rat hearts were rapidly removed, mounted on a Langendorff apparatus and subjected to 30 min ischemia followed by 30 min reperfusion with Krebs-Henseleit (K-H) solution at 37☌ to establish the isolated I/R injury model. The aim of the present study was to investigate the protective effect of baicalin (BA) against ischemia-reperfusion (I/R) injury in isolated rat hearts.
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