论文部分内容阅读
目的:研究高血糖是否可通过增加大鼠急性缺血/再灌注(I/R)心肌氧化应激而加重心肌损伤,并探讨其机制。方法:将SD大鼠随机分为3组:假手术组(Sham)、生理盐水对照组(Vehicle)和高糖组(HG)。通过缺血30 min再灌注6 h,建立大鼠急性心肌I/R模型。通过静脉输注高浓度葡萄糖溶液,建立大鼠急性心肌I/R并发高血糖动物模型。术中监测血糖水平。再灌注结束后,检测血浆心肌酶谱水平,心肌梗死面积(IS)、心肌细胞凋亡指数(AI)和caspase 3的活性,检测心肌组织中氧化应激指标超氧阴离子、gp91phox、MDA、SOD,以及硫氧还蛋白结合蛋白(Txnip)的水平和硫氧还蛋白(Trx)的活性。结果:与Vehicle组比较,HG组大鼠血糖水平显著升高,肌酸激酶(CK)、乳酸脱氢酶(LDH)的水平和IS增加,AI和caspase 3的活性升高(P<0.05)。HG组I/R心肌组织氧化应激程度显著升高,超氧阴离子、gp91phox和MDA水平增加(P<0.05)。同时,HG组I/R心肌组织的Txnip表达增加而Trx活性降低(P<0.05)。结论:高血糖可增加大鼠I/R心肌中Txnip的表达,抑制Trx的活性促进氧化应激,这可能是其加重I/R心肌损伤的机制。
AIM: To investigate whether hyperglycemia aggravates myocardial injury by increasing myocardial oxidative stress during acute ischemia / reperfusion (I / R) in rats and explores its mechanism. Methods: SD rats were randomly divided into 3 groups: sham group, saline control group and high glucose group. Acute myocardial I / R model was established by reperfusion 30 min after ischemia for 6 h. Acute myocardial I / R hyperglycemia model in rats was established by intravenous infusion of high concentration glucose solution. Intraoperative monitoring of blood glucose levels. Plasma levels of myocardial enzymes, myocardial infarct size (IS), cardiomyocyte apoptosis index (AI) and caspase 3 activity were measured after reperfusion. The levels of oxidative stress indicators such as superoxide anion, gp91phox, MDA, SOD , As well as the level of thioredoxin binding protein (Txnip) and thioredoxin (Trx) activity. Results: Compared with vehicle group, blood glucose level increased significantly in HG group. The levels of creatine kinase (CK), lactate dehydrogenase (LDH), IS and the activities of AI and caspase 3 increased (P <0.05) . HG group I / R myocardial tissue oxidative stress increased significantly, superoxide anion, gp91phox and MDA levels increased (P <0.05). At the same time, Txnip expression in I / R myocardium increased and Trx activity decreased in HG group (P <0.05). CONCLUSION: Hyperglycemia can increase the expression of Txnip in rat I / R myocardium and inhibit the activity of Trx to promote oxidative stress, which may be the mechanism of its aggravating I / R myocardial injury.