| Objective:1.To observe the dynamic changes of the myocardial protein Apelin and APJ atdifferent time points in asphyxia neonatal rats by establishing the model of neonatalrats with normobaric asphyxia, to discuss its correlation with the immaturemyocardial hypoxia ischemia injury.2.To investigate the effect of traditional chinese medicine leonurine to themyocardial hypoxia ischemia injury of asphyxia neonatal rats and its influence to theexpression of the myocardial Apelin and APJ, to discuss the specific mechanism ofthe leonurine.Methods:1.Experimental grouping and the model building: Totally72newborn healthyand clean Sprague-Dawley(SD) rats of seven day-old were randomly divided into3groups:normal group(n=24),asphyxia group(n=24), leonurine processing group(n=24).The model group SD rats were put into separably55ml container without oxygen(grinding mouth bottle, guarantee its leakproofness) which contains CaO-NaOH5g,after the animals become quiet, use vaseline daub the sealing surface, plug the bottlestopper, the mouth of bottles were sealed up for half an hour, then being given oxygen120minutes. Normal group only to simulate the process of the model of neonatal ratswith normobaric asphyxia, do not plug stopper and reoxygenation;Leonurinepreprocessing group rats were given intraperitoneal(i.p.) injection of Leo(5mg·kg-1)after the30mins of asphyxia. Then the blood and the myocardial tissues samples werecollected at three time points of30min,60min,120min (8rats at each time point)after establishing the model of neonatal rats with normobaric asphyxia, which wereused for the detection of relevant index.2.To observe the pathomorphism of myocardial tissues of each group by HEdyeing method; detect the level of blood CK,LDH; The myocardial Apelin and APJ expression activity were measured by enzyme-linked immuno sorbent assay method.3.Statistical methods:using the software SPSS13.0to do the statistical analysis,all the datas were expressed as mean±standard error (x s), and statisticalsignificance was evaluated by One-Way ANOVA between groups, the multiplecomparison was evaluated by SNK-q test, P<0.05represented that difference hadstatistics meaning.Results:1.The myocardial fine structural of neonatal rats: Compared with normal group,myocardial cells were arranged disorderly, edema and congestion happened inmyocardial stroma, infiltration of inflammatory cells can be seen in asphyxia group ateach time points. Compared with the asphyxia group at same time point, edema andcongestion of myocardial stroma and infiltration of inflammatory cells can bealleviated in leonurine preprocessing group.2.Myocardial enzyme CK of neonatal rats: Compared with normal group, thelevel of CK activity rised significantly at different time points in asphyxia group andthe leonurine processing group (P<0.01), it increased at30min, and continued to goup at60min,120min. Compared with the asphyxia group, it decreased significantly ateach time point in leonurine processing group (P<0.01).3.Serum LDH of neonatal rats: Compared with normal group, the level of LDHactivity rised significantly at different time points in asphyxia group and the leonurineprocessing group (P<0.01), it increased at30min, and continued to go up at60min,120min. Compared with the asphyxia group, it decreased significantly at each timepoint in leonurine processing group (P<0.01).4.Myocardial expression of Apelin of neonatal rats: Compared with normalgroup, the myocardial expression of Apelin activity rised significantly at differenttime points in asphyxia group and the leonurine processing group(P<0.01), itincreased at30min, reached the peak at60min, decreased at120min. Compared withthe asphyxia group, it decreased significantly at each time point in leonurineprocessing group(P<0.01).5.Myocardial expression of APJ of neonatal rats: Compared with normal group,the myocardial expression of APJ activity rised significantly at different time points in asphyxia group and the leonurine processing group(P<0.01), it was increased at30min, reached the peak at60min, and decreased at120min. Compared with theasphyxia group, it decreased significantly at each time point in leonurine processinggroup(P<0.01).Conclusions:1.The expressions of plasma creatine kinase(CK) and lactate dehydrogenase(LDH) activity and the myocardial protein Apelin/APJ were increased duringmyocardial hypoxia ischemia injury in asphyxia neonatal rats. The endogenousApelin/APJ system was involved in the pathological physiology process ofmyocardial hypoxia ischemia injury, and may have a cardioprotective effect.2.Leonurine can lessen myocardial enzyme CK,LDH, alleviate the pathologicalchanges of myocardial injury, which showed its protection to immature myocardialhypoxia ischemia injury caused by asphyxia.3.The protection of leonurine to myocardial hypoxia ischemia injury was notthrough the mechanism of directly increasing the expression of protein Apelin/APJ,meanwhile, the leonurine expressed its protection to myocardial hypoxia ischemiainjury, which may further inhibit the compensatory increased expression of Apelin/APJ. |
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