Genetic Blockade of NAAA Cell-specifically Regulates Fatty Acid Ethanolamides (FAEs) Metabolism and Inflammatory Responses
Laboratory studyOther animalsWith NAAA gene deletion (CRISPR-Cas9) or the NAAA inhibitor F96, which raise the body's own palmitoylethanolamide; PEA itself was not given
This study tested palmitoylethanolamide together with NAAA gene deletion (CRISPR-Cas9) or the NAAA inhibitor F96, which raise the body's own palmitoylethanolamide; PEA itself was not given. Its results cannot be assigned to palmitoylethanolamide alone. More combination studies.
- Design
- Laboratory study
- Subjects
- NAAA-deficient and wild-type mice, including bone marrow chimeras; numbers not stated in the abstract
- Dose used in the study
- Not stated in the abstract
- Duration
- Not stated in the abstract
- What was measured
- PEA and AEA levels in bone marrow, macrophages and lungs; inflammation in LPS-induced acute lung injury; pain in carrageenan hyperalgesia and sciatic nerve injury models
What the authors reported
The study found:
- NAAA deletion raised PEA and AEA in bone marrow and macrophages.
- Unexpectedly, gene deletion gave only moderate anti-inflammatory effects in lung injury and poor pain relief, whereas the inhibitor F96 gave marked anti-inflammation and analgesia.
- Chimera experiments showed deleting NAAA in bone marrow-derived cells produced strong effects, while absence in non-bone-marrow cells did not.
Limits of this study
A mouse study; it cannot show effect in people. No palmitoylethanolamide was given. The authors declare no commercial or financial relationships.
Source
PubMed 35069223 · doi:10.3389/fphar.2021.817603
Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.