CAJ | 학술논문

目的研究β淀粉样蛋白诱导小胶质细胞的炎性上清对神经元凋亡的影响.方法用浓度为125 hmol/L的Aβ1-42诱导的小胶质细胞炎性上清干预神经元,检测Bcl-2、Caspase-3、PARP的表达及神经元凋亡的情况.结果炎性上清液干预组Caspase-3(14.2±1.8)、Bcl-2阳性细胞数(10.6±0.8)明显高于Aβ1-42干预组(2.2±0.6,5.0±0.3)(P＜0.01),吖啶橙免疫荧光结果显示炎性上清液处理组与Aβ1-42直接干预组48 h和72 h凋亡率比较差异有统计学意义(P＜0.05).结论 Aβ1-42诱导小胶质细胞的炎性上清可以通过Caspase-3途径诱导神经元凋亡,小胶质细胞活化引起的慢性炎性过程是Aβ引起神经细胞凋亡的重要条件之一.
목적 연구β정분양단백유도소효질세포적염성상청대신경원조망적영향.방법 용농도위125 hmol/L적Aβ1-42유도적소효질세포염성상청간예신경원,검측Bcl-2、Caspase-3、PARP적표체급신경원조망적정황.결과 염성상청액간예조Caspase-3(14.2±1.8)、Bcl-2양성세포수(10.6±0.8)명현고우Aβ1-42간예조(2.2±0.6,5.0±0.3)(P＜0.01),아정등면역형광결과현시염성상청액처리조여Aβ1-42직접간예조48 h화72 h조망솔비교차이유통계학의의(P＜0.05).결론 Aβ1-42유도소효질세포적염성상청가이통과Caspase-3도경유도신경원조망,소효질세포활화인기적만성염성과정시Aβ인기신경세포조망적중요조건지일.
Objective To study the effects of neuronal apoptosis under the induction of β-amyloid inflammatory supernatant. Methods The neurons were intervened by β-amyloid-induced inflammatory supernatant at the concentration of Aβ1-42 at 125 nmol/L. And the expressions of Bcl-2, caspase-3, PARP and neuronal apoptosis were detected. Results The caspase-3 ( 14. 2 ± 1.8 ), Bcl-2 ( 10. 6 ± 0. 8 ) positive cells of microglia inflammatory supernatant stimulated group were significantly elevated than the control(2. 2 ± 0. 6,5. 0 ± 0. 3, P ＜ 0. 01 ). Nuclear chromatin was uniform yellow-green fluorescent. And there was significant difference of neuronal apoptosis between microglia inflammatory supernatant group and Aβ1-42directly stimulated group. Conclusion Neuronal apoptosis is induced by caspase-3 in β-amyloid inflammatory supernatant. One of the important causes is chronic inflammatory process of activated microglia by Aβ.