阿尔茨海默病中C1q诱导氧化神经毒性研究

Study of Complement C1q-induced Oxidative Stress in Alzheimer Disease

目的探讨补体C1q能否诱导神经元产生氧化应激反应以及Aβ对其反应的干预作用。方法采用神经元原代培养法,以Amplex-TM-Red检测氧化应激产物(ROS)的产生,MTT法检测细胞活力。结果C1q的加入在0.5、2、6h均引起了神经元ROS生成增加,其中2h达高峰,同对照组相比差异有统计学意义(P<0.05)。加入Aβ1-40抑制了C1q诱导的神经元ROS的产生。结论C1q与神经元的共育导致ROS的产生,提示C1q可能是导致脑内神经元氧化毒性及神经元死亡的因素之一,而加入Aβ1-40可阻断ROS的生成。

Objective To investigate the induction of C1q on the oxidative stress from neurons and the intervention effect of Aβ 1-40. Methods Primary neuron culture was adopted. The Amplex-TM-Red was adopted to detect the production of Reactive Oxygen Species（ROS） from neurons. MTT method was used to detect the cell viability. Results C1q addition induced the enhancement of ROS from neurons at 0.5, 2, 6 hour. The ROS reached peak at 2 hour which was significantly different from the control group（P〈0.05）. Aβ 1-40 addition inhibited the ROS production induced by C1q. Conclusions The coincubation of C1q and neurons induced ROS production which was reduced by Aβ 1-40. It was indicated that C1q was the key factor of oxidative stress in AD pathogenesis.