摘要
目的探讨脂质载体前列腺素E1(liposomal prostaglandin E1,Lipo-PGE1)抗心肌缺血-再灌注损伤的可能机制。方法用结扎冠状动脉的方法制备在体心肌缺血-再灌注损伤模型,将大鼠随机分为3组:假手术组、模型组、Lipo-PGE1保护组。用酶联免疫和放射免疫法测定缺血-再灌注损伤后血妊娠相关血浆蛋白-A(PAPP-A)、肿瘤坏死因子-a(TNF-a)的含量;亚硝酸盐比色测定血清超氧化物歧化酶(SOD)活性,TBA荧光显色法测定脂质过氧化物(LPO)含量;发色底物显色法测定组织型纤溶酶原激活物(t-PA)及纤溶酶原激活物抑制剂(PAI-1);计算心肌梗死范围。结果与模型组相比,Lipo-PGE1保护组梗死面积减小(P<0.01),模型组PAPP-A、TNF-a浓度明显高于假手术组(P<0.01),Lipo-PGE1组PAPP-A、TNF-a浓度明显低于模型组(P<0.01);血清LPO含量明显降低,SOD活性显著升高(P<0.01);Lipo-PGE1提高t-PA活性,降低PAI-1活性(P<0.01)。结论Lipo-PGE1通过减少炎症因子的产生、增加SOD活力、降低LPO含量和提高纤溶功能而保护缺血-再灌注损伤的心肌。
Objective To investigate the mechanism of Lipo-PGE1 against myocardial ischemia/reperfusion injury（IRI）. Methods The IRI models of rats were established by hgating the left anterior coronary artery for 45 min and then reperfusion the heart for 120 min. Healthy male Waster rats were divided randomly into 3 groups（9 in each group） ： Ⅰ sham-operated groups, Ⅱ IRI groups and Ⅲ Lipo-PGE1 groups. The levels of PAPP-A and TNF-a were detected respectively by the methods of ELISA and radioimmunoassay. The activity of SOD was measured by nitrite colormatric assay. The concentration of LPO was detected by TBA fluoreacence. The levels of t-PA and PAI-1 were measured by amidolytical assay. Results Compared with sham-operated groups, the infarcted area of Lipo-PGE1 groups was decreased. The levels of PAPP-A, TNF-ain IRI groups were higer than sham-operated groups obviously（P 〈 0.01 ）. The levels of PAPP-A,TNF-a in Lipo-PGE1 groups were higer than IRI groups obviously（ P 〈 0.01 ）. The level of LPO was decreased, but the activity of SOD was increased. Lipo- PGE1 could elevate the activity of t-PA and decrease the activity of PAI-1 （ P 〈 0.01 ）. Conclusion Lipo-PGE1 could protect myocardium against the ischemia/reperfusion injury by decreasing the outcoming of inflammory factor,increaslng the activity of SOB,decreasing the lever of LPO and enhancing the function of fibrinolysis.
出处
《中国实验诊断学》
2006年第3期255-257,共3页
Chinese Journal of Laboratory Diagnosis
基金
吉林省卫生厅科研基金资助课题(046)
