Background: This study evaluated the protective effect of Echinatin against myocardial ischemia/reperfusion (I/R)\ninjury in rats.\nMethods: The effect of Echinatin on cardiac function in rats subjected to I/R was demonstrated through improved\nLangendorff retrograde perfusion technology. Adult Spragueââ?¬â??Dawley rats were randomly divided into five groups,\nand myocardial infarct size was macroscopically estimated through 2,3,5-triphenyltetrazolium chloride staining.\nThe coronary effluent was analyzed for the release of lactate dehydrogenase (LDH) and creatine kinase (CK)\nto assess the degree of cardiac injury. The concentrations of malondialdehyde (MDA), interleukin-6 (IL-6), and\ntumor necrosis factor-Ã?± (TNF-Ã?±) were determined along with superoxide dismutase (SOD) activity using ELISA.\nFinally, cardiomyocyte apoptosis analysis was conducted with POD, an in situ cell death detection kit.\nResults: Echinatin (0.5 and 2.5 Ã?¼g/mL) pretreatment enhanced the maximum up/down rate of the left ventricular\npressure (Ã?±dp/dtmax), improved the heart rate, increased the left ventricular developed pressure (LVDP), enhanced\nthe coronary flow, and reduced the CK and LDH levels in the coronary flow of the treated group compared with the\nI/R group. Echinatin limited the contents of CK and LDH, improved the LVDP, reduced the contents of MDA, IL-6, and\nTNF-Ã?±, and increased the SOD activity. The infarct size and cell apoptosis in the hearts of the rats in the\nEchinatin-treated group were smaller and lower, respectively, than those in the hearts of the rats in the I/R\ncontrol group.\nConclusion: Echinatin exerts a protective effect against I/R-induced myocardial injury on hearts. This effect\nmay be attributed to the antioxidant and anti-inflammatory activities of this compound
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