硼替佐米对大鼠脑缺血再灌注损伤的保护机制研究

发布时间：2018-01-04 04:44

本文关键词：硼替佐米对大鼠脑缺血再灌注损伤的保护机制研究　出处：《韶关学院学报》2016年10期 　论文类型：期刊论文

更多相关文章： 硼替佐米 脑缺血再灌注损伤 Bax 凋亡

【摘要】：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(P0.05);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(P0.05).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.
[Abstract]:In order to protect the mechanism of bortezomib on cerebral ischemia reperfusion injury in rats. 45 rats were randomly divided into sham operation group, model group and bortezomib prevention group, 15 rats in each group. Model group and bortezomib prevention group ischemia reperfusion model was established, including bortezomib in the prevention group 2 h before ischemia. Intraperitoneal injection of bortezomib. Surgical operation in sham group were the same, but the suture only entered 10 mm. rats in the ischemia-reperfusion brain tissue was taken out after 24 h, using TTC staining to observe infarct size, expression of immunohistochemical staining was used to detect Bax protein. The results showed that: TTC staining showed that the sham operation group without cerebral infarction the model group, and bortezomib prevention group had cerebral infarction, but the prevention group was significantly less than the area of infarction model group (P0.05); immunohistochemical staining showed that compared with sham operation group, bortezomib prevention group Bax protein expression increased significantly, but weaker than the model group (P0.05) can be considered. Bortezomib has a protective effect on cerebral ischemia-reperfusion injury, one of its mechanisms may be that it inhibits apoptosis of nerve cells.

【作者单位】：韶关学院医学院临床医学系;
【基金】：广东省大学生创新训练项目(1057613-04)
【分类号】：R743.3
【正文快照】： 脑缺血再灌注后,脑组织局部过度的炎症反应和细胞凋亡过多等是造成脑组织再灌注损伤的原因[1-2],而蛋白酶体对很多参与炎症反应和凋亡通路的蛋白都具有重要的调节作用[3-4].硼替佐米又名“万坷”,是一种蛋白酶体抑制剂,对癌症有一定的治疗作用[5],目前临床上主要用于多发性骨

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