雌激素对Aβ25-35致PC12细胞膜流动性改变的影响

目的观察可溶性Aβ25-35作用下PC12细胞膜流动性的改变及17β-雌二醇(17βE2)对此改变的影响。方法培养的PC12细胞分为空白对照组,Aβ损伤组及雌激素干预组,根据浓度梯度雌激素干预组再分为5个剂量亚组,采用荧光偏振法动态检测不同组PC12细胞不同时间膜流动性的改变。结果Aβ损伤组在加入5μmol/L可溶性Aβ25-35后各时间点,与空白对照组比较,其微黏度η值均明显升高(P<0.01);17βE2干预组在10-10mol/L浓度的条件下各时间点η值与Aβ损伤组比较差异无显著性(P>0.05);而在10-9~10-6mol/L浓度的条件下各时间点η值与Aβ损伤组比较均显著降低(P<0.01),且这种作用具有剂量依赖性,17βE210-91、0-8、10-7、10-6mol/L干预组与Aβ损伤组比较,在24 h时PC12细胞微黏度η值分别降低了36.4%、49.6%、60%及68.4%。结论可溶性Aβ25-35 5μmol/L使PC12细胞微黏度明显升高,膜流动性明显下降;雌激素具有改善膜流动性保护神经元的作用,且这种作用具有剂量依赖性。

Effect of estrogen on the change of PC12 cell membrane fluidity induced by Aβ25-35

Objective To investigate the change of PC12 cell membrane fluidity under the effect of soluble Aβ25-35 and the influence of 17βE_2 on the change.Methods The cultured PC12 cells were divided into three groups,i.e.the blank group,the Aβ damaged group and the 17βE_2 intervention group.The 17βE_2 intervention group was subdivided into five subgroups according to concentration gradients of 17βE_2.The changes of PC12 cell membrane fluidity in different groups at different time were dynamically detected by means of fluorescence polarization.Results Compared with the blank group,after adding 5 μmol/L of soluble Aβ25-35,the microviscosity values η of Aβ damaged group increased significantly(P<0.01) at each time point.Compared with the Aβ damaged group,at 10~(-10) mol/L concentration of 17βE_2,the values η of the 17βE_2 intervention group showed no significant difference(P>0.05);while at 10~(-9)～10~(-6) mol/L concentrations,the values η decreased significantly(P<0.01 or P<0.05) at each time point and in a dose-dependent manner compared with the Aβ damaged group.Compared with those in the Aβ damaged group,the PC12 cell microviscosity values η of the 17βE_2 10~(-9),10~(-8),10~(-7),10~(-6)mol/L intervention groups at 24h decreased by 36.4%,(49.6%,)60% and 68.4% respectively.Conclusion 5μmol/L of soluble Aβ25-35 makes the microviscosity of PC12 cell remarkably increase and the membrane fluidity remarkably decrease.Estrogen has neuron-protecting function by improving membrane fluidity,and this function is dose-dependent.