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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
Summary
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.
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.
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