Notch1受体在脑缺血损伤中表达变化及作用的体外研究

Expression and effects of Notch1 in an in vitro model of cerebral ischemia

目的观察Notch1受体在脑缺血损伤中的表达变化及其配体Jagged1对缺血损伤的影响,探讨Notch信号通路可能参与脑缺血损伤的机制。方法建立PC12诱导的神经元样细胞氧糖剥夺(OGD)体外脑缺血模型,应用Real-time PCR及Western-blot技术,检测OGD 3h、6h、9h、12h、16h、24h Notch1表达变化;MTT法检测外源性配体Jagged1对细胞缺血损伤的影响。结果与对照组相比,OGD后不同时间Notch1 mRNA及蛋白的表达量均有显著升高,3h时达最高峰,其后随OGD时间的延长逐渐下降,OGD 24h达最低点(P<0.05)。分别与对照组比较,外源性Jagged1干预可使正常及缺血神经元存活率均下降(P<0.05)。结论 Notch信号转导通路可能通过内源性的Notch1受体表达上调参与脑缺血性损伤过程。

Objective To investigate the Notchl expression in PC12 cells subjected to ischemia injury and the effects of exogenous Jaggedl in vitro. Methods Neuron like cells induced from PC12 cells subjected to the oxygen/glucose deprivation （OGD） was introduced as an in vitro brain ischemia model. Expression of Notchl was examined with reahime PCR and Western-blot;method of MTr was used to investigate the effect of Jaggedl on cell survival. ResuLts Realtime PCR and Western analysis show that Notchl expression increased significantly than control group and reached the peak after 3h of OGD, then decreased gradually（ P 〈 0.05 ） , and exogenous Jaggedl augment the isehemia injury. Conclusion Notch signaling pathway may be involved in the process of brain injury by the endogenous up-regulation of Notchl.