Azelnidipine Attenuates the Oxidative and NFκB Pathways in Amyloid-β-Stimulated Cerebral Endothelial Cells

Tao Teng, Devin M. Ridgley, Andrey Tsoy, Grace Y. Sun, Sholpan Askarova, James C. Lee

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Cerebral amyloid angiopathy (CAA), a condition depicting cerebrovascular accumulation of amyloid β-peptide (Aβ), is a common pathological manifestation in Alzheimer's disease (AD). In this study, we investigated the effects of Azelnidipine (ALP), a dihydropyridine calcium channel blocker known for its treatment of hypertension, on oligomeric Aβ (oAβ)-induced calcium influx and its downstream pathway in immortalized mouse cerebral endothelial cells (bEND3). We found that ALP attenuated oAβ-induced calcium influx, superoxide anion production, and phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and calcium-dependent cytosolic phospholipase A 2 (cPLA 2 ). Both ALP and cPLA 2 inhibitor, methylarachidonyl fluorophosphate (MAFP), suppressed oAβ-induced translocation of NFκB p65 subunit to nuclei, suggesting that cPLA 2 activation and calcium influx are essential for oAβ-induced NFκB activation. In sum, our results suggest that calcium channel blocker could be a potential therapeutic strategy for suppressing oxidative stress and inflammatory responses in Aβ-stimulated microvasculature in AD.

Original languageEnglish
Pages (from-to)209-215
Number of pages7
JournalACS Chemical Neuroscience
Issue number1
Publication statusPublished - Jan 16 2019


  • Alzheimer's
  • Amyloid-β peptide
  • Azelnidipine
  • NFκB
  • cytosolic phospholipase A
  • endothelial cells

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Cognitive Neuroscience
  • Cell Biology


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