摘要
目的探讨凝血酶(Thrombin,TM)脑内注射对周围组织Caspase-3蛋白表达和细胞凋亡的影响。方法TM、TM+组织蛋白酶G(Cathepsin G,CATG)、TM+Caspase-3抑制剂(DEVD-fmk)脑内立体定向注射制作动物模型,应用Western-blot技术检测Caspase-3蛋白表达,TUNEL法检测细胞凋亡。结果TM脑内注射后6hCaspase-3蛋白开始增加,与对照组比较差异具有显著性(P<0.01),注射后24h达高峰(P<0.01),然后逐渐下降,96h时恢复至正常水平;TM脑内注射后24h凋亡细胞数目开始增加,与对照组比较差异具有显著性(P<0.05),48h达高峰(P<0.01),然后逐渐下降。TM+DEVD-fmk脑内注射后凋亡细胞数目与对照组比较差异无显著性(P>0.05)。TM+CATG脑内注射后Caspase-3蛋白表达和凋亡细胞数目与对照组比较差异均无显著性(P>0.05)。结论TM通过蛋白酶激活受体-1(protease activated receptor-1,PAR-1)激活Caspase-3,诱导细胞凋亡。
Objective To explore the effect of thrombin（TM） on caspase-3 protein expression and apoptosis after intracerebral injection in rats. Methods TM,TMq-CATG or TM＋DEVD-fmk was stereotaxically injected into right caudate nucleus in rats. Caspase-3 protein expression determined by Western-blot method. Apoptosis of cells was measured by TUNEL method. Results Caspase-3 protein expression was increased at 6h after TM in tracerebral injection （P〈0. 05） ,peaked at 24h（P〈0.01） ,and then declined. Cells of apoptosis increased at 24h af ter TM intracerebral injection（P〈0.05） ,peaked at 48h（P〈0. 01） ,and then declined. Cells of apoptosis had no sig- nificant difference as compared with control group after TM＋DEVD-fmk intracerebral injection. Caspase-3 protein expression and cells of apoptosis had no significant difference as compared with control group after TM＋CATG intracerebral injection. Conclusion Thrombin activates caspase-3 by PAR-1 and then induces apoptosis.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2006年第6期655-657,共3页
Journal of Apoplexy and Nervous Diseases
