应用PC12细胞模型研究环氧化酶-2在帕金森病发病机制中的作用

The role of Cyclooxygenase-2 in the pathogenesis of Parkinson's disease in the study with PC12 celluar model

目的探讨环氧化酶-2(COX-2)在帕金森病(PD)发病机制中的作用。方法利用腺病毒载体将COX-2导入PC12细胞使其高表达COX-2,为实验验组;未导入COX-2的PC12细胞为对照组。两组细胞经神经生长因子(NGF)诱导后成为多巴胺能神经元,然后加入6-羟多巴(6-OHDA)诱导建立帕金森病细胞模型。分别用LDH方法和流式细胞术(FCM)检测两组细胞的损伤程度以确定COX-2是否可以作为独立因素影响PD的发病机制。结果LDH和FCM结果均显示实验组细胞损伤程度明显高于对照组(P<0.01)。结论COX-2可以提高神经元对于6-OHDA毒性的敏感性。

Objective To discuss the role of cyclooxygenase-2 （COX-2） in the pathogenesis of Parkinson＇ s disease （PD）. Methods Experimental group consisted of PC12 cells which highly express COX-2 transfected by adenovirus vector. Control group included only PC12 cells. Both groups were induced by nerve growth factor（NGF） to differentiate into doperminergic neurons. Then adding 6-hydroxydopamine （6-OHDA） into the culture, cellular model of PD was established. Lactate dehydrogenase（LDH） and flow cytometry（ FCM ） detection were administered to estimate the extent of cellular injury in order to find out whether COX-2 could influence the pathogenesis of PD as an independent factor. Result Both LDH and FCM detections showed the extent of celluar injury in the experimental group was much higher than that in control group （P 〈 0.01 ）. Conclusion COX-2 could elevate the sensitivity of neurons to the toxcity induced by 6-OHDA.