| Objective: Being the simplest amino acid, glycine not only acts as an anti-endotoxin agent, but also has great effects on cytoprotection. It has been demonstrated that glycine protected against myocardial injury induced by endotoxin and acute ischemia in our laboratory works. For contributing to the treatment for ischemic heart disease, the aim of this study was to investigate the protection of glycine against myocardial ischemia-reperfusion and its mechanism.Methods: Mice were randomly divided into five groups and fed with different solution (0.25mL/10g, twice per day). On the 8th day, the mice were injected with pituitrin (30U/kg) and nitroglycerin (10mg/kg, 30 min later) intraperitoneally to remodel acute myocardial ischemia-reperfusion (MI/R). ECG and heart rate were recorded at Omin, 5min, lOmin, 20min, 30min, 40min, 50min. 4h later, the activities of nitric oxide synthase, inducible nitric oxide synthase, and concentrations of nitric oxide in myocardium were examined; The expression of Bcl-2 mRNA in myocardium was also determined by RT-PCR.Results: J point of ECG and heart rate decreased obviously in MI/R-injured mice. Compared to Group MI/R, J point of ECG and heartrate decreased smoothly in Group MI/R+GLY (P<0.05, P<0.01). The activities of NOS and concentrations of NO in Group MI/R+GLY were higher than those in Group MI/R (P<0.01), but the activities of iNOS was lower inversely (P<0.01). In addition, the expression of Bcl-2 mRNA in Group MI/R+GLY was higher than that in Group MI/R (P<0.01).Conclusions: The results suggested that pretreatment of glycine attenuated myocardial ischemia-reperfusion injury induced by pituitrin and nitroglycerin. The mechanism may be related to NOS activation, the increase of NO content, the expression of Bcl-2 mRNA, and the reduction of iNOS in I/R-injured myocardium. |
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