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

Xiao Jing Sun, Lei Zhao, Na Zhao, Xiao Li Pan, Guo Qiang Fei, Li Rong Jin, Chun Jiu Zhong

Research output: Contribution to journalArticlepeer-review


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. The Aβ 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.

Original languageEnglish (US)
Pages (from-to)561-566
Number of pages6
JournalNeuroscience Bulletin
Issue number5
StatePublished - Oct 2012


  • Alzheimer's disease
  • Benfotiamine
  • Glycogen synthase kinase-3
  • High glucose
  • β-amyloid

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology


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