维生素E对糖尿病大鼠心肌缺血再灌注损伤的影响

目的观察糖尿病大鼠心肌缺血再灌注(MIR)时细胞间粘附分子-1(ICAM-1)和自由基代谢的变化及维生素E对其的影响。方法通过腹腔注射链脲佐菌素制作糖尿病大鼠模型,造模成功后4w进行MIR处理。糖尿病大鼠30只分为假手术对照(sham)组,MIR组和维生素E(VE)治疗组。免疫组织化学法检测心肌ICAM-1蛋白表达。检测血清、心肌组织SOD、GSH-Px活性、MDA含量和活性及心肌线粒体Na+,K+-ATP酶、Mg++-ATP酶、Ca++-ATP酶活性。结果与sham组相比,MIR组心肌线粒体Na+,K+-ATP酶、Mg++-ATP酶、Ca++-ATP酶活性明显下降;血清、心肌MDA明显升高,血清、心肌SOD和GSH-Px活性明显降低用,心肌ICAM-1蛋白表达明显升高;用VE4w后与MIR组比,心肌线粒体Na+,K+-ATP酶、Mg++-ATP酶活性明显升高;血清、心肌MDA降低,血清、心肌SOD和GSH-Px活性升高,心肌ICAM-1蛋白表达降低。结论维生素E可通过减轻脂质过氧化和自由基损伤,下调ICAM-1蛋白表达,拮抗糖尿病大鼠心肌缺血再灌注损伤。

EFFECTS OF VITAMIN E ON MYOCARDIAL ISCHEMIC REPERFUSION INJURY IN DIABETIC RATS

Objective To observe the effects of vitamin E(VE) on the changes of the intercellular adhesion molecule-1(ICAM-1)and free radicals in ischemic-reperfused myocardium(MIR) of diabetic rats Method The diabetic rat model was established by i.p.streptozotocin injection.Four weeks later,MIR models were established,and 30 rats were divided into three groups with each group 10 rats(sham group,MIR group and VE group).The ICAM-1 protein expressions were evaluated by immunocytochemistry.The contents of malonialdehyde(MDA) in serum and myocardial tissues were detected.The activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) in serum and myocardial tissues were measured.The activities of Na+,K+-ATPase,Mg++-ATPase,Ca++-ATPase in myocardial mitochondria were measured.Results Compared with sham group,the activities of Na+,K+-ATPase,Mg++-ATPase,Ca++-ATPase in myocardial mitochondria were decreased,the contents of MDA in serum and myocardium increased,the levels of SOD and GSH-Px in serum and myocardium decreased,and the levels of ICAM-1 in myocardium increased significantly in MIR group.Compared with MIR group,the activities of Na+,K+-ATPase,Mg++-ATPase in myocardial mitochondria were increased,the levels of MDA in serum andmyocardium decreased the activities of SOD and GSH-Px in serum and myocardium increased,and the levels of ICAM-1 in myocardium decreased significantly in VE group.Conclusion VE could relieve myocardial ischemic reperfusion injury and the damage of lipid peroxidation and free radical induced by MIR in diabetic rats,and this effect was mediated by reduction of the expression of ICAM-1 protein.