晚期糖基化终产物在β样淀粉蛋白25-35诱导PC12细胞氧化损伤中的作用

Effect of advanced glycation end products on the oxidative damage of PC12 cells induced by amyloid beta protein 25-35

目的探讨晚期糖基化终产物(AGEs)在β样淀粉蛋白25-35(Aβ25-35)诱导PC12细胞氧化损伤中的作用。方法将实验对象分为五组:10、20、304、0μmol/L四种浓度的Aβ25-35干预组和正常对照组。采用MTT法测定细胞生存率,采用ELISA法测定AGEs的含量。结果Aβ25-35诱导PC12细胞,细胞生存率为50%时,Aβ25-35浓度约为30μmol/L;与正常对照组相比,30μmol/L Aβ25-35干预组细胞生存率明显降低(P<0.001)、细胞内AGEs含量明显升高(P<0.05)。结论AGEs参与了β样淀粉蛋白25-35诱导PC12细胞氧化损伤的过程。

Objective To investigate the effect of advanced glycafion end products （AGEs） on the oxidative damage of PC12 coils induced by amyloid beta protein 25 - 35 （Aβ25 - 35）- Methods There are five groups including the normal group and four intervention groups with different concentrations of Aβ25 - 35 （ 10,20,30,40 μmol/L）. Survival rate of PC12 cells was detected by MTF assays, the content of AGEs by ELISA. Results During the precess of cell necrosis induced by Aβ25- 35, the concentration of Aβ25 - 35 was 30 μmol/L when coil growth rate of PC12 was 50% .Compared with the normal group, survival rate of PC12 cells in the intervention group with 30 μmol/L Aβ25- 35 was decreased （P 〈 0. 001 ）, and contents of AGEs were increased （ P 〈 0.05）. Conclusion AGEs plays a certain role in the process of oxidative damage induced by Aβμ25- 35.