| ObjectivesAlzheimer's disease (AD) is one of the most critical health problems for aged people all over the world. Deposition ofβ-amyloid (Aβ) in the brain is considered as the major cause for the development of AD. Senile plague (sp) that developed by Aβdeposition in extracellular cells has been proved to be the typical feature of neuropathology for AD. Based on the above amyloid hypothesis, our current study was designed to investigate the effect of gastrodin on Aβdeposition in 293sw and APP695 cells which with over-expressed amyloid precursor protein (APP). And we aim to provide a possible clinical treatment strategy for AD patients.MethodsTwo cell lines, 293sw and APP695, were treated with different concentration of gastrodin. The vitality of the cells was then detected by MTT. The morphological feature of the cells was assessed by the usage of light microscope. Besides, the stability of the cells pretreated with gastrodin was determined by immunohistochemistry, and Aβconcentration in culture medium was detected by ELISA. Lastly, protein levels of APP and IDE in cells, and Aβin culture medium, precipited with TCA-DOC were detected by Western Blot.ResultsGastrodin, at concentration of 25-200umol/l, could increase cell vitality without affecting cell growth. No significant pathological alteration was observed in the cells treated with gastrodin, in comparison with control. In addition, ELISA and Western Blot data indicated that Aβsecretion was significantly reduced under the treatment of different concentration of gastrodin. However, no change was detected on IDE activity.ConclusionGastrodin could decrease the secretion of Aβthrough inhibiting the expression of APP in 293sw and APP695 cells, indicating a potential neuro-protective role of gastrodin in the treatment of AD through a non-IDE pathway. Thus, our present study provides a potential strategy to the clinical treatment of AD.
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