酪氨酸激酶和蛋白激酶C参与高铁血红素诱导的抗大鼠心肌缺血再灌注损伤  

Involvement of Tyrosine Kinase and Protein Kinase C in Hemin Reduces Ischemia/Reperfusion Injury in Rat Hearts

作　　者：汪洋[1] 徐和靖[2] 王万铁[1] 陈莹莹[3] 沈岳良[3] 杜友爱[2] 

机构地区：[1]温州医学院病理生理学教研室,浙江省温州市325035 [2]温州医学院生理学教研室,浙江省温州市325035 [3]浙江大学医学院生理学教研室,浙江省杭州市310006

出　　处：《中国动脉硬化杂志》2007年第2期93-96,共4页Chinese Journal of Arteriosclerosis

基　　金：浙江省教育厅科研基金(20041095)

摘　　要：目的研究酪氨酸激酶和蛋白激酶C参与高铁血红素诱导血红素氧合酶1在对抗心肌缺血再灌注损伤中的作用及其机制。方法离体大鼠心脏行Langendorff灌流,给予30min缺血和2h再灌注,观察心室收缩功能、乳酸脱氢酶、肌酸激酶和心肌梗死面积等指标。结果腹腔注射高铁血红素24h后,可明显改善缺血再灌注心脏的收缩功能,减少再灌注期乳酸脱氢酶和肌酸激酶释放,缩小心肌梗死面积。在腹腔注射高铁血红素前给予酪氨酸激酶抑制剂Genistein和蛋白激酶C抑制剂Chelerythrine可阻断高铁血红素引起的心肌梗死面积缩小和心功能的改善。结论高铁血红素可诱导血红素氧合酶1活性增加并对抗心肌缺血再灌注损伤,其作用与酪氨酸激酶和蛋白激酶C的激活有关。Aim To investigate tyrosine ldnase （TK） and protein kinase C （PKC） are related to hemin, a heme oxygenase- 1 （ HO- 1 ） inducer, reduces ischemia/repeffusion （ I/R ） injury and which mechanisms are involved in the cardioprotective effects. Methods Infarct size was measured in isolated rat hearts following occlusion of the left anterior descending coronary artery for 30 min and subsequent reperfusion for 2 h. The ventricular function, lactate dehydrngenase （ LDH） and creatine kinase （ CK） during ischemia/repeffusion period were also observed. Results Infarct size, LDH and CK were reduced in the hemin （50 mierograms/kg） group compared with the control group. The myocardial performance was also improved in heroin group. Both Genistein, the inhibitor of PTK and Chelerythrine, the inhibitor of PKC blocked the infarct size-limiting effect and improvement in myocardial performance induced by hemin. Conclusion These data suggest that the involvement of PTK and PKC have been implicated in hemin-induced cardioprotection in rat hearts.

关 键 词：病理生理学 血红素氧合酶1 高铁血红素 酪氨酸激酶 蛋白激酶C 缺血再灌注 

分 类 号：R363[医药卫生—病理学]