Protective Effect of Sufentanil against Myocardial Ischemia Reperfusion Injury in Rats
Protective Effect of Sufentanil against Myocardial Ischemia Reperfusion Injury in Rats
Peixia Yu1*, Lijun Bo2 and Xueyin Song1
ABSTRACT
The objective of this study was to investigate the action of sufentanil (Fen) pretreatment on inducible myocardial apoptosis by ischemia-reperfusion (I/R) in rats. 120 male rats (mean age = 3 months) were randomly assigned to six conditions: control group (group S), I/R group, normal saline (NS) I/R group, and low, medium and high dose Fen groups, where in high dose group: Fen1:2μg/kg; Fen2:4μg/kg; Fen3:6μg/kg. The measured items included heart rate (HR), mean arterial pressure (MAP), left ventricular developed pressure (LVDP), ±dp/dtmax, malondialdehyde (MDA), superoxide dismutase (SOD) activity, creatine phosphokinase MB (CK-MB) and cardiac troponin-I (cTnI). The total apoptotic cardiomyocytes, B cell lymphoma 2 (Bcl-2) and Bax protein and mRNA expression were detected in the myocardial ischemia (MI) region. The HR and the MAP of the Fen group exceeded that of the I/R group, while the LVDP and ±dp/dtmax were approximate to the basic values. The MDA concentrations and CK-MB values of the Fen group went down and the SOD activity went up when was compared with the I/R group. Whereas, cTnI concentrations of Fen1 and Fen2 groups sharply decreased (all P<0.05); the myocardial injury of the Fen group was less the I/R group. Whereas, the MI region and apoptosis indexes of Fen1 and Fen2 groups dropped significantly (all P<0.05); moreover, Bcl-2 protein and mRNA expression rose significantly in the Fen group by being compared to the I/R group, while Bax protein and mRNA expression were declined clearly (all P<0.05). Regulating Bcl-2 and Bax of Fen pretreatment can inhibit I/R-induced myocardial apoptosis of rats. As a result, Fen may be a potential drug to treat of I/R injury-related heart disease.
To share on other social networks, click on any share button. What are these?
