论文部分内容阅读
目的观察电刺激小脑顶核(FN)对持续局灶性脑缺血钙蛋白酶活性的影响,以阐明其神经保护作用机制。方法健康雄性Wistar大鼠,随机分为假手术组(PO)、FN刺激假手术组(PO-FN)、持续缺血组(PI)及持续缺血-FN刺激组(PI-FN),后两组又分为缺血1,3,6,12及24h组。建立大鼠电刺激FN及持续局灶性脑缺血模型,应用Western印迹半定量各组缺血核心区Mr=150000FBDP含量(表示钙蛋白酶活性),并应用尼氏体染色对缺血核心区神经元数量及形态进行分级评分。结果PO组及PO-FN组钙蛋白酶活性相似(P>0.05),处于低水平。PI组钙蛋白酶活性从缺血1h犤(3670±600)A/μg总蛋白犦开始即显著增高(t=6.338,P<0.001),以后随着缺血时间延长,钙蛋白酶活性不断增高,直至缺血24h犤(9180±360)A/μg总蛋白犦仍有持续增高趋势(缺血12,24h,t=14.673,16.632,P<0.001)。PI-FN组随着缺血时间的延长,钙蛋白酶活性从缺血1h犤(2510±460)A/μg总蛋白犦也开始增高,以后随着缺血时间延长,钙蛋白酶活性不断增高,但各时点组与其相应PI组相比,其增高程度明显减低,差别具有显著意义(缺血1,24h,t=1.875,2.134,P<0.05)。PO组及PO-FN组神经元形态及数量正常,评分均为0分。PI组从缺血1h(0.8±0.3)开始,神经元形态、数量即出现轻度改变,其评分增高(z=2.443,P<0.01),以
Objective To observe the effects of electrical stimulation of fastigial nucleus (FN) on the activity of calpain in permanent focal cerebral ischemia in order to clarify its neuroprotective mechanism. Methods Healthy male Wistar rats were randomly divided into sham-operation group (PO), FN-stimulated sham operation group (PO-FN), continuous ischemic group (PI) and continuous ischemic-FN stimulation group Two groups were divided into ischemia 1, 3, 6, 12 and 24h groups. The models of electrical stimulation FN and continuous focal cerebral ischemia were established. Western blotting was used to semi-quantitatively determine the content of Mr = 150000FBDP in each ischemic core region (indicating calpain activity). Nissl staining The number and morphology of grading. Results The activity of calpain in PO group and PO-FN group was similar (P> 0.05), and was at a low level. The activity of calpain in PI group was significantly increased from 1 36 μg / ml to 366 μg / kg total protein (t = 6.338, P <0.001), and later with the prolongation of ischemia, the activity of calpain increased continuously 24hours after ischemia (9180 ± 360) A / μg total protein titers continued to increase (ischemia12,24h, t = 14.673,16.632, P <0.001). With the prolongation of ischemia time, the activity of calpain also increased from 1h 犤 (2510 ± 460) A / μg total protein PI in the PI-FN group, and later with the prolongation of ischemia, the calpain activity increased continuously Compared with the corresponding PI group at each time point, the increase was significantly lower (P <0.05). The difference was significant (ischemia 1,24h, t = 1.875,2.134, P <0.05). The morphology and number of neurons in PO group and PO-FN group were normal, with a score of 0. In the PI group, neuronal morphology and quantity changed slightly from 1 h after ischemia (0.8 ± 0.3), and its score increased (z = 2.443, P <0.01)