本文關(guān)鍵詞：線粒體自噬在阿爾茨海默病細(xì)胞模型中的作用機(jī)制，，由筆耕文化傳播整理發(fā)布。

線粒體自噬在阿爾茨海默病細(xì)胞模型中的作用機(jī)制

Mechanism of mitophagy in a cell model of Alzheimer＇s disease

[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11]

ZHAO Xuelian;YU Jun;XIE Zhaohong;CAO Yanjun;LIU Zhen;WANG Xiao;XU Linlin;YANG Hui;ZHENG Xiaolei;SHEN Yang;BI Jianzhong （ 1. Department of Neurology, the Second Hospital of Shand

[1]山東大學(xué)第二醫(yī)院神經(jīng)內(nèi)科,山東濟(jì)南250033; [2]山東中醫(yī)藥大學(xué)附屬醫(yī)院,山東濟(jì)南250011

文章摘要：目的 研究阿爾茨海默病細(xì)胞模型20E2自噬情況及其可能機(jī)制。方法 應(yīng)用ELISA檢測體外培養(yǎng)的HEK293細(xì)胞和20E2細(xì)胞（穩(wěn)定轉(zhuǎn)染APPSW的HEK293細(xì)胞）上清Aβ1-40水平、Western blotting檢測APP蛋白表達(dá)水平,確定20E2細(xì)胞是否建模成功。電鏡下觀察細(xì)胞內(nèi)線粒體,JC-1檢測兩種細(xì)胞線粒體膜電位,流式細(xì)胞儀檢測細(xì)胞凋亡情況。Western blotting檢測LC3-II、PINK1、Parkin表達(dá)水平。結(jié)果 與HEK293細(xì)胞相比,20E2細(xì)胞APP蛋白、Aβ1-40表達(dá)增加（P〈0.05）,線粒體腫脹、嵴消失、空泡化明顯,線粒體膜電位下降,PINK1、Parkin、自噬相關(guān)蛋白LC3-II表達(dá)增加（P〈0.05）。結(jié)論 阿爾茨海默病細(xì)胞模型20E2線粒體形態(tài)改變明顯、膜電位下降,這些改變可能通過PINK1、Parkin途徑引起線粒體自噬增加。

Abstr：Objective To investigate the effect of autophagy involved in Alzheimer＇s disease cell model 20E2 and its possible mechanism. Methods To determine whether the 20E2 cells model was successfully established,we detected the levels of Aβ1-40 in HEK293 cells and 20E2 cells（ HEK293 cells stably expressing Swedish mutant APP） cultured in vitro by ELISA kit,and the expression of APP protein level was detected by Western blotting. The mitochondria in cells was observed by electron microscope. The mitochondrial membrane potential of both cells was detected by fluorescence probe JC-1. Flowcytometry was used to measure the apoptotic rate. LC3-II,PINK1 and Parkin were detected by Western blotting. Results The expression levels of APP protein and Aβ1-40 increased in 20E2 cells compared with those in HEK293 cells. Mitochondrial swollen,cristae disappeared and vacuolization was obviously observed. Mitochondrial membrane potential decreased. The expression levels of PINK1,Parkin and LC3-II increased（ P〈0. 05）. Conclusion In Alzheimer＇s disease cell model 20E2,the mitochondrial morphology changed obviously and membrane potential of mitochondria declined,and these changes may cause the increase of mitochondrial autophagy through PINK1 and Parkin pathway.

文章關(guān)鍵詞：

Keyword：:Alzheimer＇s disease Mitophagy Mitochondrial membrane potential PINK1 Parkin

課題項(xiàng)目：國家自然科學(xué)基金（81371420,81171214,81401052）;山東省自然科學(xué)基金（ZR2011HM064）;山東省衛(wèi)生廳科研項(xiàng)目（2013WS0248）

作者信息：會員可見

  本文關(guān)鍵詞：線粒體自噬在阿爾茨海默病細(xì)胞模型中的作用機(jī)制，由筆耕文化傳播整理發(fā)布。