人尿激肽原酶在急性脑梗死大鼠模型中的研究

Research of human urinary kallidinogenase on acute cerebral infarction in rats

目的探讨人尿激肽原酶对急性脑梗死大鼠模型的作用机制。方法应用线拴法构建大脑中动脉栓塞致急性脑梗死大鼠模型,并随机分为实验组及模型对照组。实验组经腹腔注射人尿激肽原酶(3.5×10-3 PNAU/kg),模型对照组同法予以生理盐水(10ml/kg),应用免疫组化法分别检测两组梗死灶区微血管密度;应用蛋白质印迹杂交检测两组凋亡相关蛋白Bcl-2的表达,应用AO/EB法检测梗死灶区神经细胞的凋亡率。结果实验组MVD(84.450±5.104条/HP)高于模型对照组MVD(57.900±3.370条/HP);实验组的Bcl-2蛋白表达水平明显高于模型对照组;实验组细胞凋亡率较模型对照组明显降低。结论人尿激肽原酶可使大鼠脑梗死灶中微血管密度增加;应用人尿激肽原酶后大鼠脑梗死灶中细胞凋亡蛋白Bcl-2表达明显增加,脑细胞凋亡受到抑制,脑细胞凋亡率降低。

Objective To discuss the mechanism of human urinary kallidinogenase on acute cerebral infarction in rats. Methods By suture method we build the rat model with acute cerebral infarction,were randomly divided the rats into the experimental group and the model control group. The experimental group was injected human urinary kallikrein （3.5 × 10^-3 PNAU/kg） by intraperitoneal injectinon,which model control group was injected physiological saline by intraperitoneal injection （10 ml/kg）. Rats were sacrificed 7 days after modeling. We cut issue infarction area through operation,and detected the infarctarea of MVD by immuno histochemical method in experimental group and model control group. We detected the expression of apoptosis relat- ed protein Bcl-2 with the application of Western blot hybridization （Western blot） in experimental group and control group. At the same time,we detected the apoptosis rate of the nerve cells in infarct with the AO/EB method,and statistical analysis was performed using SPSS software. Results MVD in experimental group were 84. 450±5. 104 / HP and 57. 900±3. 370 / HP in control group（ P〈0.05 ）. Bcl-2 expression in experimental group was higher than that of model control group. The cell apopto- sis rate in experimental group was decreased obviously compared with model control group. Conclusion Experiments bad estab- lished that human urinary kallidinogenase could increase the microvascular density in acute cerebral infarction in rats. Human u- rinary kallidinogenase obviously increased the apoptosis protein expression of Bcl-2 in infarction in rats,and brain cells apoptosis was restrained and brain ceils apoptosis rate reduced.