硼替佐米对大鼠脑缺血再灌注损伤的保护机制研究

The Pretective Effect of Bortezomib on Cerebral Ischemia-reperfusion Injury Rats

为探讨硼替佐米对脑缺血再灌注损伤的保护机制.将45只大鼠随机分成假手术组、模型组和硼替佐米预防组,每组15只.模型组和硼替佐米预防组建立缺血再灌注模型,其中硼替佐米预防组在缺血前2 h腹腔注射硼替佐米.假手术组的手术操作相同,但线栓只进入10 mm.各组大鼠在再灌注24 h后取脑组织,用TTC染色观察梗死面积,免疫组化染色检测Bax蛋白的表达.结果表明:TTC染色显示假手术组没有脑梗死灶,模型组和硼替佐米预防组有脑梗死,但预防组梗死面积要明显小于模型组(P<0.05);免疫组化染色显示,与假手术组相比,硼替佐米预防组Bax蛋白表达显著增强,但要弱于模型组(P<0.05).可以认为硼替佐米对脑缺血再灌注损伤具有保护作用,其机制之一可能是其抑制了神经细胞凋亡.

In order to probe into the protective effect and mechanism of Bortezomib in cerebral ischemia-reperfusion injury nerve cells.45 rats randomly divided into three groups, sham-operation group, model group and bortezomib prevention group with 15 rats in each group. In the model group and the bortezomib prevention group, it made rats middle cerebral artery ischemia-reperfusion models. And two hours before ischemia the bortezomib prevention group was given bortezomib by intraperitoneal injection. Most of operation among these three groups are the same, except sham-operation group which strings were inserted into ten millimetre. Finally, it took rats brain tissue which were used to observe infarct size by TTC dye and detect Bax protein expression by immunohistochemistry dye from each group. Results showed that as it is shown from TTC dye result, there are no cerebral infarction in sham-operation group. The area of cerebral infarction of bortezomib prevention group is smaller than model group. The expression of Bax protein in bortezomib prevention group is stronger than sham-operation group but weaker than model group. Conclusions were that Bortezomib had protective effect of the nerve cells of cerebral ischemia-reperfusion injury rats, and probably preventing apoptosis pathway was one of its mechanism.