| Objective: Currently myocardial infarction (MI) is a common disease in China, and theincidence is rising. Ca2+overload after MI is an important factor causing myocardial cellinjury, and Ca2+-CaM-CaMKⅡ signal system plays an important role in controlingintracellular Ca2+cycle, CaMKⅡ may be an effective treatment target onorganic cardiopathy. But the signaling pathway which is cored on cardiac CaMK Ⅱisunclear. Taurine (Tau) plays a regulatory role on intracellular Ca2+homeostasis, howeverits specific regulatory mechanism is unclear too. Therefore, this study is aimed atrevealing the change rule of CaMKⅡ protien level and discussing the relation betweenTau’s cardioprotective effects and CaMKⅡ,by testing CaMKⅡ content at different timepoints and the changes of myocardial tissue and CaMKⅡprotien level after given Tautreatment.Methods: Animal model of AMI was produced by ligating the left anteriordescending coronary artery (LAD) of the rats. Rats were assigned to3groups of sham,control and medicated group. Animals were sacrificed at time points of24h,1w,3wrespectively, observing changes and the effects of Tau on CaMKⅡ content andmyocardium infarction area; simultaneously the effect of Tau on ischemic myocardiumcell morphology was observed by HE staining, and CaMKⅡexpression was measured byPCR.Results：After the ligation of left anterior descending coronary artery, the control groupshows the typical ST segment elevation, proved that myocardial infarction model copy issuccessful.The medicated group were given Tau right after ligation.24h,7d and21d，the medicated group’s electrocardiogram improved significantly compared with thecontrol, taurine treatment group of ECG ST segment elevation range is lower than thecontrol;The myocardium infarction area of taurine treatment group significantly isnarrowed compared with control group. After24h the expression of CaM and CaMKIIdelta mRNA were lower in control group and taurine treatment inhibits that. Taurineinhibits the inhibition of CaMK Ⅱ protein expression after myocardial infarction.After3w, the CaMKII protein level in control group was higher than the sham group, but theprotein level was close in medicated group and sham group.24h taurine treatment groupdecreases the expression of protein P53and P21, and reduces the the level of activativecaspase3, then protects myocardial cells.Conclusion：Tau probably inhibited myocardial cell apoptosis at early acute myocardialinfarction and inhibited CaMK Ⅱ overexpression at late acute myocardial infarction byregulating CaMK Ⅱ transcription and protein activity. |
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