Effect of Huperzine A on Aβ-induced p65 of astrocyte in vitro

Biosci Biotechnol Biochem. 2016 Dec;80(12):2334-2337. doi: 10.1080/09168451.2016.1222265. Epub 2016 Aug 24.

Abstract

Alzheimer's disease (AD) is the most common cause of dementia. Its pathology often accompanies inflammatory action, and astrocytes play important roles in such procedure. Rela(p65) is one of significant message factors in NF-κB pathway which has been reported high expression in astrocyte treated by Aβ. HupA, an alkaloid isolated from Chinese herb Huperzia serrata, has been widely used to treat AD and observations reflected that it improves memory and cognitive capacity of AD patients. To reveal its molecular mechanisms on p65, we cultured astrocytes, built Aβ-induced AD model, treated astrocytes with HupA at different concentrations, assayed cell viability with MTT, and detected p65 expression by immunohistochemistry and PCR. Our results revealed that treatment with 10 μM Aβ1-42 for 24 h induced a significant increase of NF-κB in astrocytes; HupA significantly down-regulated p65 expression induced by Aβ in astrocytes. This study infers that HupA can regulate NF-κB pathway to treat AD.

Keywords: Alzheimer’s disease; Huperzine A; astrocyte; p65.

MeSH terms

  • Alkaloids / pharmacology*
  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Astrocytes / drug effects*
  • Astrocytes / metabolism*
  • Mice
  • Peptide Fragments / pharmacology*
  • Sesquiterpenes / pharmacology*
  • Transcription Factor RelA / metabolism*

Substances

  • Alkaloids
  • Amyloid beta-Peptides
  • Peptide Fragments
  • Rela protein, mouse
  • Sesquiterpenes
  • Transcription Factor RelA
  • amyloid beta-protein (1-42)
  • huperzine A