The protection and related mechanism of morroniside in rat model of myocardial ischemic reperfusion injury

Objective To investigate the effect of morroniside on myocardial ischemia reperfusion injury (MIRI) in a rat model of myocardial ischemic reperfusion injury and reveal the possible mechanisms behind it. The obvervational index mainly include the expression of the apoptosis gene Bcl-2 and Bax, the infarction area percentage, the tissue section and the myocardial enzyme. Methods Healthy male Sprague Dawley rats were randomly allocated to three groups:sham, ischemia/reperfusion (IR) and morroniside. The group of IR and morroniside are made ischemia reperfusion injury (IRI) models through surgery. Serum creatine kinase isoenzyme (CK-MB) were assayed. The infarct size was determined by triphenyl tetrazolium chloride staining. The tissue section are observed through microscope. The apoptosis gene Bax and Bcl-2 was assessed through real-time polymerase chain reaction. Results Compared with the sham group, the infarct size percentage, the serum creatine kinase isoenzyme (CK-MB) level, the damage of tissue and the Bax and Bcl-2 gene expression level were significantly raised in the IRI and morroniside group. Compared with the IR group, the infarct size percentage, the serum creatine kinase isoenzyme (CK-MB) level, the damage of tissue and the Bax gene expression level were significantly reduced in the morroniside group, while Bcl-2 gene expression level was significantly increased. Conclusion This experiment demonstrate that morroniside provides an enhanced protection against myocardial IRI and may through the Bcl-2-linked apoptotic signaling pathway.