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Related Experiment Video

Updated: Feb 13, 2026

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
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Sulforaphane rescues amyloid-β peptide-mediated decrease in MerTK expression through its anti-inflammatory effect in

Kyoung A Jhang1, Jin-Sun Park2, Hee-Sun Kim3

  • 1Department of Microbiology, Division of Molecular Biology and Neuroscience, School of Medicine, Ewha Medical Research Institute, Ewha Womans University, Seoul, 158-710, Republic of Korea.

Journal of Neuroinflammation
|March 14, 2018
PubMed
Summary
This summary is machine-generated.

Amyloid-beta (Aβ) reduces Mer tyrosine kinase (MerTK) expression, increasing inflammation in Alzheimer's disease. Sulforaphane prevents this by inhibiting NF-κB, suggesting MerTK targeting for AD therapeutics.

Keywords:
Alzheimer’s diseaseAβ1-42Innate immune responseMerTKSulforaphane

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Mer tyrosine kinase (MerTK) dysregulation is implicated in Alzheimer's disease (AD) chronic inflammation.
  • The mechanism of amyloid-beta (Aβ)-mediated MerTK regulation in inflammation is unclear.

Purpose of the Study:

  • To elucidate the mechanism of Aβ-mediated MerTK downregulation.
  • To investigate the modulatory effect of sulforaphane on MerTK expression in Aβ-challenged macrophages.

Main Methods:

  • Utilized THP-1 macrophages stimulated with Aβ1-42.
  • Employed Ca2+ imaging, Western blotting, and siRNA knockdown.
  • Assessed MerTK expression, cytokine production, and NF-κB activation.

Main Results:

  • Aβ1-42 decreased MerTK expression and increased IL-1β and TNF-α via intracellular Ca2+ and NF-κB activation.
  • Sulforaphane inhibited Aβ1-42-induced inflammation and MerTK downregulation by blocking NF-κB.
  • MerTK knockdown diminished sulforaphane's anti-inflammatory effects, confirming MerTK's role.

Conclusions:

  • Aβ1-42-induced neuroinflammation is mediated by MerTK downregulation.
  • Sulforaphane, by targeting MerTK, shows therapeutic potential for AD.