参附注射液对心肌缺血再灌注损伤患者Bcl-2、Bax与Caspase-3蛋白水平的影响

Influence of Shenfu Injection on Protein Levels of Bcl-2,Bax and Caspase-3 of Myocardial Ischemia Reperfusion Injury Patients

目的:探讨参附注射液对心肌缺血再灌注损伤患者Bcl-2,Bax与Caspase-3蛋白水平的影响。方法:将40例急性心肌梗死患者按随机数字表法分为两组。对照组20例采用溶栓治疗,观察组20例在溶栓治疗前后均给予参附注射液静脉滴注,6 d为1个溶栓疗程,疗程结束后比较两组患者的冠脉再通率以及采用酶联免疫吸附测定(ELISA)检测两组患者血浆中Bcl-2、Bax与Caspase-3蛋白水平。结果:①观察组的冠脉再通率明显高于对照组(P<0.05);②两组再灌注损伤发生率比较,差异有统计学意义(P<0.05);③观察组患者血浆中Bax、Caspase-3蛋白水平明显低于对照组(P<0.05),而Bcl-2表达水平明显高于对照组(P<0.05)。结论:参附注射液治疗心肌缺血再灌注损伤的作用机制与抑制心肌细胞凋亡有关。

Objective：To explore the influence of Shenfu Injection on protein levels of Bcl-2, Bax and Caspase-3 of myocardial ischemia reperfusion injury patients. Methods ：40 patients with acute myocardial infarction were divided into two groups according to random num- ber table method, each of 20 cases. The control group was given thrombolytic therapy, and the observation group was treated with Shenfu Injection intravenous infusion before and after thrombolytic therapy. 6 days as a course of thrombolysis treatment. The reperfusion rate of coronary artery of the two groups patients were compared and protein levels of Bcl-2, Bax and Caspase-3 of the two groups were detected by enzyme-linked immunosorbent assay （ELISA） after treatment. Results：（1）Coronary rate of observation group was obviously higher than that of control group （ P 〈 0.05 ） ;（2）The reperfusion rate of coronary artery of the observation group was obviously higher than that of the control group （ P 〈 0.05 ） ; Comparison the reperfusion injury incidence of the two groups showed that the observation group was lower than the control group and the difference was statistically significant（ P 〈 0.05 ） ;（3）Protein levels of Bax and Caspase-3 in the observation group were significantly lower than that of the control group （ P 〈 0.05 ）, while Bcl-2 expression level was significantly higher than the control group （ P 〈 0.05 ）. Conclusion ： The mechanism of Shenfu Injection in treating myocardial ischemia reperfusion injury is related to the inhibition of myocardial cell apoptosis.