Tier 4 — mechanistic

Inhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide-induced microglial and astrocytic neuroinflammation by increasing NAD+

Jureepon Roboon, Tsuyoshi Hattori, Hiroshi Ishii, Mika Takarada-Iemata, Dinh Thi Nguyen, Collin D Heer, Denis O'Meally, Charles Brenner, Yasuhiko Yamamoto, Hiroshi Okamoto, Haruhiro Higashida, Osamu Hori
Journal of Neurochemistry 2021 158(2):311-327

Bibliography

PubMed
PMID 33871064
PubMed Central
PMC8282715
Funding
Indexed grant support includes NCI NIH HHS. The complete funding declaration is not specified in the accessible abstract.
Competing interests
A complete competing-interest declaration is not specified in the accessible publication information.

Study snapshot

DesignIn vivo mouse and primary-cell mechanistic study
ModelLPS-induced neuroinflammation in mice and primary microglia/astrocytes
SampleLPS-challenged mice and primary glial cultures
InterventionApigenin as a CD38 inhibitor and nicotinamide riboside as an NAD+ precursor
DurationPretreatment and inflammatory challenge protocols
EndpointsNAD+ levels; Microglial and astrocytic activation; Inflammatory cytokines; CD38-related signaling

What the study showed, in plain terms

This study tested whether inhibiting CD38 with apigenin or supplying an NAD+ precursor could blunt experimental neuroinflammation.

Key findings

In the experimental models, apigenin increased NAD+ and reduced LPS-induced inflammatory activation in microglia and astrocytes, supporting a CD38/NAD+-linked mechanism.

What this study can and cannot tell us

The findings are preclinical. They do not establish that oral apigenin raises brain NAD+ or treats neuroinflammatory disease in humans.

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