Sphingosine Kinases at the Intersection of Pro-Inflammatory LPS and Anti-Inflammatory Endocannabinoid Signaling in BV2 Mouse Microglia Cells
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- BV2 mouse microglia cell line challenged with LPS
- Dose used in the study
- URB597 (FAAH inhibitor) or JWH133 (CB2 agonist); palmitoylethanolamide itself was not added
- Duration
- Not stated in the abstract
- What was measured
- TNF-alpha and IL-1beta production, levels of anandamide and related lipids including PEA, and transcription of the sphingosine kinases SphK1 and SphK2.
What the authors reported
This laboratory study found:
- URB597 prevented LPS-induced TNF-alpha and IL-1beta and caused accumulation of anandamide, PEA and other ethanolamides.
- JWH133 mimicked the effect of URB597.
- LPS induced SphK1 and SphK2, and inhibiting either kinase strongly reduced cytokine production.
- Both URB597 and JWH133 prevented LPS-induced SphK1 and SphK2 transcription.
Limits of this study
A mouse cell line study; it cannot show effect in people or animals. PEA rose as one of several lipids after FAAH inhibition and was not tested alone. The authors declare no conflict of interest.
Source
PubMed 37239854 · doi:10.3390/ijms24108508
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.