OBJECTIVE: To investigate the effect and mechanism of contracture inhibitor 2,3-butanedione monooxime in improving abnormal calcium injury in isolated rat hearts.
Methods: Thirty-two SD male rats were randomly divided into 4 groups: normal control group, BDM control group, abnormal calcium group and BDM intervention group. The isolated rat heart was subjected to Langendorff perfusion to record left ventricular pressure (LVP), left ventricular end-diastolic pressure (LVEDP), and calculate left ventricular developed pressure (LVDP). ) to evaluate cardiac function; determine the content of lactate dehydrogenase (LDH) in coronary effluent during reperfusion to reflect myocardial injury; 2, 3, 5-triphenyltetrazolium chloride (TTC) staining method to evaluate myocardial infarction area Cardiomyocyte apoptosis index was detected by TUNEL method; expression of cleaved caspase-3 and cytochrome c protein was detected by Western blot method.
Results: Compared with the normal control group, there were no significant changes in the left ventricular function, myocardial infarction area and apoptosis index, and the expressions of cleaved caspase-3 and cytochrome c protein in the BDM (20 mmol/L) control group ( P>0.05); in the abnormal calcium group, LVEDP was significantly elevated, LVDP was 0, LDH content in coronary effluent was significantly increased (P<0.01), the="" expressions="" of="" cleaved="" caspase-3="" and="" cytochrome="" c="" protein="" apoptosis="" index="" were="" significantly="" increased="" p="">0.05).<0.01), almost all cardiac tissues died (P<0.01); BDM (20 mmol/L) intervention group with abnormal calcium significantly reduced the myocardial infarction area (P<0.01), decreased LVEDP, and partially recovered LVDP (P<0.01). 0.01), decreased LDH release (P<0.01), cleaved caspase-3 and cytochrome c protein expression and apoptosis index were significantly decreased (P<0.01).
Conclusion: BDM can significantly inhibit contracture and apoptosis caused by acute calcium overload, improve cardiac function, and alleviate calcium overload injury in isolated rat hearts. It is a potential ischemia-reperfusion cardioprotective drug.