Tier 4 — mechanistic

Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38

Knut Husø Lauritzen, Kuan Yang, Michael Frisk, Mieke C. Louwe, Maria Belland Olsen, Mathias Ziegler, William E. Louch, Bente Halvorsen, Pål Aukrust, Arne Yndestad, Øystein Sandanger
Frontiers in Immunology 2025 15:1497984

Bibliography

PubMed
PMID 39840045
PubMed Central
PMC11746122
DOI
10.3389/fimmu.2024.1497984

Study snapshot

DesignEx vivo human-cell and mouse-cell mechanistic study
ModelPrimary human monocytes and monocyte-derived macrophages; wild-type and CD38-knockout mouse macrophages
Sample
InterventionApigenin before NLRP3 activation with ATP, MSU or nigericin
Duration
EndpointsIL-1β release; TNF release; Gasdermin-D; Calcium flux; Cellular NAD+; CD38 dependence

What the study showed, in plain terms

This study tested whether apigenin suppresses NLRP3 inflammation because it inhibits CD38.

Key findings

Apigenin reduced NLRP3-dependent IL-1β release and calcium flux, but still worked in CD38-deficient macrophages. Acute apigenin treatment did not raise NAD+ in the tested human macrophages.

What this study can and cannot tell us

These are mechanistic cell data, not clinical anti-inflammatory evidence. The findings also show that apigenin's actions cannot be reduced to a single CD38 mechanism.

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology