Aβ25-35损伤对Hep-1细胞内质网分子伴侣GRP78表达的影响

摘要

目的 构建阿尔茨海默病(AD)内皮细胞损伤模型,探讨β-淀粉样蛋白损伤对血管内皮细胞内质网分子伴侣含量的影响.方法 体外培养内皮细胞瘤Hep-1细胞株,应用Aβ25-35构建AD细胞模型,应用免疫荧光染色,激光共聚焦显微镜下观察细胞内内质网分子伴侣含量变化.结果 经Aβ25-35诱导的Hep-1 AD细胞内质网分子伴侣GRP78表达增加.结论 β-淀粉样蛋白损伤后血管内皮细胞细胞内分子伴侣含量上调可能为其参与AD发病的机制之一.%Objective The purpose of this study was to detect the expression of ER molcculal chaporonc GRP78 after β amyloid protein injury in Hep 1 cells. Methods Aβ25 35 was used to build the Hep 1 ecll model of AD. Immunofluos ecnec staining was used to dctcet the amount of moloeular rh.iporono GRI'78. Results The expression of ER molecular chaporono GRP78 was inercased in immortal human ondothelial cells (Hep 1) after injury induced by Aβ25 35. Conclusion Incrcased β amyloid protcin production should up regulate signaling of the unfolded protein responde (UPR) were pathological mechanisms relate to AI.