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目的通过抑制细胞周期素依赖激酶(Cyclindependentkinases,CDKS)来对神经元凋亡进行干预,以探讨细胞周期调控与细胞凋亡的关系。方法建立光化学法诱导大鼠局灶性脑缺血模型,并随机分为脑缺血组(对照组和干预组)和假手术组,采用HE染色显示梗死灶,并测定其面积占脑片面积百分率的平均值;通过TUNEL方法检测神经元凋亡;免疫印迹(Westernblot)观察损伤侧皮层周期素蛋白A(CyclinA)和周期素蛋白B1(CyclinB1)的表达。结果缺血后24h对照组梗死灶面积占脑片面积百分率的平均值明显大于干预组(P<0.05),缺血后梗死灶周围可见大量TUNEL阳性染色细胞,且对照组数量明显多于干预组(P<0.05),二者均多于假手术组(P<0.05);缺血后24h干预组大鼠NeuN+TUNAL双标阳性表达率明显弱于对照组大鼠(P<0.05);Westernblot显示对照组CyclinA和CyclinB1的表达明显高于干预组(P<0.05)。结论细胞周期抑制剂可部分抑制缺血边缘区神经元的凋亡及减小脑梗死面积,这提示细胞周期调控可能参与了神经细胞的凋亡过程。
Objective To investigate the relationship between cell cycle regulation and apoptosis by inhibiting the apoptosis of neurons by inhibiting the expression of cyclindependent kinases (CDKS). Methods A rat model of focal cerebral ischemia induced by photochemistry was established and randomly divided into cerebral ischemia group (control group and intervention group) and sham operation group. Infarcted foci were observed by HE staining and the area of brain slice area Neuronal apoptosis was detected by TUNEL method. The expression of CyclinA and CyclinB1 in injured cortex was detected by Western blotting. Results The infarct size in the control group was significantly higher than that in the intervention group (P <0.05), and the number of TUNEL-positive cells in the control group was significantly more than that in the intervention group (P <0.05), both of which were more than those of the sham-operation group (P <0.05). The positive rate of NeuN + TUNAL double staining in 24h intervention group was significantly weaker than that in the control group (P <0.05) The results showed that the expression of CyclinA and CyclinB1 in the control group was significantly higher than that in the intervention group (P <0.05). Conclusion Cell cycle inhibitors can partially inhibit the apoptosis of ischemic neurons in the marginal zone and decrease the infarct size. This suggests that cell cycle regulation may be involved in the apoptosis of neural cells.