Zn~(2+)诱导金属硫蛋白表达对大鼠缺血再灌注心肌的保护作用

目的　探讨Zn2 + 诱导金属硫蛋白表达对离体大鼠缺血再灌注 (I/R)损伤心肌的保护作用及其机制。方法　 32只Sprague Dawley大鼠随机分为 4组 :对照组、I/R组、Zn2 + 预处理组、心肌组织细胞外信号调节的蛋白激酶 (ERK)抑制剂PD980 5 9+Zn2 + 预处理组 (每组各 8只 )。分别检测心肌细胞乳酸脱氢酶 (LDH)及肌酸激酶 (CK)漏出量、心肌组织三磷酸腺苷 (ATP)含量及心功能指标 (LVSP与±dp/dtmax) ,用10 9Cd/血红素饱和法测量心肌组织中金属硫蛋白的含量。结果　与I/R组比较 ,Zn2 + 预处理组金属硫蛋白表达量增高 (P <0 0 1) ,心肌细胞LDH与CK漏出量降低 ,而心肌组织ATP增高 ,心功能指标改善 (P <0 0 1) ;Zn2 + 预处理组与对照组比较 ,两组间的LDH、CK、ATP、LVSP与±dp/dtmax差异无显著性。ERK抑制剂PD980 5 9取消Zn2 + 预处理组的上述心肌保护作用。结论　Zn2 + 诱导金属硫蛋白表达减轻大鼠心肌I/R损伤 ,其机制涉及丝裂原激活的蛋白激酶 (MAPK)途径

Protective effects of metallothionein induced by Zn2+ on ischemia/reperfusion myocardium in isolated rat heart

AIM To investigate the protective effects of metallothionein induced by Zn 2+ on ischemia/reperfusion myocardium in isolated rat heart. METHODS 32 Sprague-Dawley rats were randomly divided into 4 groups (n=8, respectively): control group, ischemia/reperfusion (I/R) group, Zn 2+ pretreated group (ZPC), PD98059 (inhibitor of extracellular signal regulated protein kinase)+Zn 2+ pretreated group (PZPC). The levels of creatime kinase (CK), lacatate dehydrogenase (LDH) and adenosine triphosphate (ATP), which indicated myocardium injury, and the cardiac function(LVSP and±dp/dt max), were observed in this study. The expression levels of MT were valued by the 109Cd/hemoglobin affinity assays. RESULTS The expression level of MT was higher in ZPC group than in control group and I/R group. Compared with I/R group, the level of LDH and CK was reduced, ATP content was increased, and cardiac function (LVSP and±dp/dt max) was improved (P<0.01) in ZPC group. The correspond data between ZPC group and control group had no significant difference. While the protective effects of ZPC were inhibited by PD98059. CONCLUSION High expression of MT induced by Zn 2+ has protective effects on ischemia/reperfusion myocardium in isolated rat hearts. This may olne to activity of mitogen activated protein kinase pathway.