CAJ | 학술논문

目的：探讨(-)表没食子儿茶素没食子酸酯( epigal-locatechin-3-gallate, EGCG)对 APP/PS1转基因小鼠学习记忆障碍的改善作用及其对海马内p75 NTR信号通路及其介导的神经细胞凋亡的影响。方法以Morris水迷宫及被动避暗实验观察其行为学变化,TUNEL法及fluoro-Jade B法检测神经细胞凋亡及神经元退行性变,并以Western blot法检测小鼠海马p75 NTR相关蛋白的表达水平。结果 EGCG可明显改善APP/PS1转基因小鼠的学习记忆障碍,抑制神经细胞凋亡及退行性改变。同时, EGCG 可明显抑制 p75 NTR通路,降低其剪切产物 p75 ICD表达及 JNK2磷酸化水平,减少p53和cleaved-caspase 3蛋白表达,从而抑制神经细胞凋亡和改善学习记忆障碍,发挥神经保护作用。结论 EGCG通过抑制p75 NTR信号通路,抑制神经细胞凋亡,改善学习记忆障碍。
목적：탐토(-)표몰식자인다소몰식자산지( epigal-locatechin-3-gallate, EGCG)대 APP/PS1전기인소서학습기억장애적개선작용급기대해마내p75 NTR신호통로급기개도적신경세포조망적영향。방법이Morris수미궁급피동피암실험관찰기행위학변화,TUNEL법급fluoro-Jade B법검측신경세포조망급신경원퇴행성변,병이Western blot법검측소서해마p75 NTR상관단백적표체수평。결과 EGCG가명현개선APP/PS1전기인소서적학습기억장애,억제신경세포조망급퇴행성개변。동시, EGCG 가명현억제 p75 NTR통로,강저기전절산물 p75 ICD표체급 JNK2린산화수평,감소p53화cleaved-caspase 3단백표체,종이억제신경세포조망화개선학습기억장애,발휘신경보호작용。결론 EGCG통과억제p75 NTR신호통로,억제신경세포조망,개선학습기억장애。
Aim To investigate whether EGCG treat-ment ameliorates cognitive deficits in APP/PS1 trans-genic mice and, whether it has the ameliorating effect of p75 NTR signaling to neuronal apoptosis in the hippo-campus of APP/PS1 mice. Methods Morris water maze test and locomotivity test were used to predict be-havioral changes; further TUNEL staining and Fluoro-Jade B staining were applied to confirm the neuronal apoptosis and neuronal degeneration;Western blot was employed to detect protein expression levels of p75 NTR signaling in the hippocampus of APP/PS1 mice. Re-sults EGCG treatment dramatically ameliorated the cognitive impairments, and inhibited the neuronal ap-optosis in the APP/PS1 mice. Moreover, EGCG treat-ment dramatically inhibited the p75 NTR signaling by de-creasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression. Conclusion EGCG treatment dramatically ameliorates the cognitive impairments, and inhibits the neuronal apoptosis by in-hibiting the p75NTR signaling.