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Benfotiamine prevents increased β-amyloid production in HEK cells induced by high glucose

Neuroscience Bulletin 2012年第5期28卷 561-566页

作者： Xiao-Jing Sun Lei Zhao Na Zhao Xiao-Li Pan Guo-Qiang Fei Li-Rong Jin Chun-Jiu Zhong Department of Neurology Zhongshan Hospital & Shanghai Medical College Fudan University Shanghai 200032 China State Key Laboratory of Medical Neurobiology Institute of Brain Science Fudan University Shanghai 200032 China

Objective To determine whether high glucose enhances β-amyloid （Aβ） production in HEK293 Swedish mutant （APPsw） cells with Aβ precursor protein （APP） overexpression, and whether under this condition benfotiamine reduces the increased Aβ production. Methods HEK293 APPsw cells were cultured with different concentrations of glucose for different times. TheAβ content in the supernatant was determined by ELISA. To investigate the mechanism by which benfotiamine reduced Aβ production, glycogen synthase kinase-3 （GSK-3） activity and expression were measured after the cells were cultured with 5.5 g/L glucose for 12 h. Results With 1.0, 3.0, 4.5, 5.5, 6.5, 7.5, 8.5, or 10.5 g/L glucose, Aβ production by HEK293 APPsw cells was highest in the presence of 5.5 g/L glucose for 6 and 12 h. The difference in Aβ content between 5.5 and 1.0 g/L was most marked after incubation for 12 h. Benfotiamine at 20 and 40 μg/mL significantly reduced Aβ production in cells incubated with 5.5 g/L glucose for 12 h. Moreover, 40 μg/mL benfotiamine significantly enhanced the ratio of phosphorylated GSK-3 to total GSK-3, together with consistent down-regulation of GSK-3 activity. Conclusion High glucose increases Aβ production by HEK293 APPsw cells while benfotiamine prevents this increase. This is correlated with the modulation of GSK-3 activity.

关键词： Alzheimer’s disease β-amyloid high glucose benfotiamine glycogen synthase kinase

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