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机构地区:[1]中国医科大学附属盛京医院心脏外科,沈阳110004
出 处:《中国医科大学学报》2012年第9期788-790,794,共4页Journal of China Medical University
基 金:辽宁省自然科学基金资助项目(20092107)
摘 要:目的探讨促红细胞生成素(EPO)预处理对缺血再灌注的大鼠心肌组织热休克蛋白70(HSP70)及细胞外信号调节蛋白激酶(ERK1/2)表达的影响及其可能的机制。方法建立大鼠在体缺血再灌注模型,结扎左前降支动脉30 min,松解2 h。24只大鼠随机分为3组,每组8只。假手术组:建模前24 h腹腔注射生理盐2 mL;对照组:建模前24 h腹腔注射生理盐水2 mL;EPO组:建模前24 h腹腔注射EPO(5 000 U/kg)。假手术组开胸手术,左前降支动脉下只穿线不结扎。RT-PCR方法分析左心室心肌组织HSP70和ERK1/2 mRNA的表达,并分析HSP70 mRNA和ERK1/2 mRNA表达量的关系。结果 EPO组HSP70mRNA表达(0.850±0.066)较盐水对照组(0.355±0.043)显著升高(P<0.01);EPO组ERK1/2 mRNA(1.150±0.125)较盐水对照组(0.576±0.116)表达水平显著升高(P<0.01);EPO预处理组大鼠的心肌组织HSP70与ERK1/2 mRNA表达量呈显著正相关(r=0.965,P<0.01)。结论 EPO预处理能够促进缺血再灌注心肌组织HSP70及ERK1/2 mRNA的表达,HSP70表达量与ERK1/2mRNA表达量呈显著正相关。Objective To study the expression of HSP70,ERK 1/2 and their possible links to the effects of EPO preconditioning.Methods A rat model of myocardial I-R injury was established by ligating the left descending coronary artery for 30 min and then reperfusing for 2 hours.Totally 24 rats were randomly divided into 3 groups:sham operation group(ip saline 2 mL,24 hours before the operation,n = 8),control group(ip saline 2 mL,24 hours before the operation,n = 8),and EPO group(ip EPO,5 000 U/kg,diluted in 2 mL of saline solution,24 hours before the operation,n = 8).The sham-operated group was subjected to thoracotomy and passage of a silk ligature around the LCA without ligation.The Expression of HSP70 mRNA and ERK1/2 mRNA in the left ventricle were analyzed by RT-PCR,and the correlation between HSP70 mRNA and ERK1/2 mRNA expression was analyzed.Results HSP70 mRNA levels in the EPO preconditioning group(0.850±0.066)were significantly higher than control group(0.355±0.043,P 〈 0.01)and sham-operated group(0.083±0.017,P 〈 0.01);ERK1/2 mRNA in the EPO group(1.150±0.125)were significantly higher than control group(0.576±0.116,P 〈 0.01)and sham-operated group(0.044±0.010,P 〈0.01);The correlation between HSP70 mRNA and ERK1/2 mRNA was significan(t r =0.965,P 〈 0.01).Conclusion A single ip injection of 5 000 units/kg of EPO at 24 hours pre-ligation enhanced the expression of HSP70 and ERK1/2 in rat myocardium,and that the possible mechanism for the increasing of HSP70 is the increased expression of ERK1/2.
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