The purpose of this study was to observe the effect of beta-amyloid protein injury on intracellular calcium homeostasis in Hep-1 cells. A beta(25-35) was used to build the Hep-1 cell model of AD. Intracellular Calcium measurements was performed by incubation with the calcium indicator probe and then observed under laser confocal microscopy. Ca2+ release from intracellular stores was significantly increased in immortal human endothelial cells (SK-Hep-1) after injury induced by A beta(25-35). No significant difference was found in CCE from injured cells to controls. Increased beta-amyloid protein production and intracellular calcium homeostasis disturbance were pathological mechanisms relate to AD.