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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Sulforaphane rescues amyloid-β peptide-mediated decrease in MerTK expression through its anti-inflammatory effect in human THP-1 macrophages

Fig. 8

Proposed mechanisms for beneficial effects of sulforaphane against decreased MerTK expression following Aβ1-42 insult in human THP-1 macrophages. Sulforaphane attenuates Aβ1-42-induced MerTK reduction through inhibiting intracellular Ca2+ overload and NF-κB signaling as replicated by EGTA and BAY 11-7082. Consequently, sulforaphane rescues a decrease of MerTK expression following Aβ1-42 stimulation, thereby inhibiting overproduction of IL-1β and TNF-α. Interestingly, Αβ1-42-induced IL-1β and TNF-α could act as negative feedback regulators of MerTK expression as confirmed with neutralizing antibodies against IL-1β or TNF-α, implicating that MerTK downregulation and induction of IL-1β and TNF-α by Aβ1-42 stimulation are interdependent. Depletion of MerTK with siRNA significantly suppressed the sulforaphane’s anti-inflammatory activities against Aβ1-42, implicating a pivotal role of MerTK for the negative regulation of the innate immune response elicited by Aβ1-42 in human THP-1 macrophages

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