Genetic Knockout of Fatty Acid Amide Hydrolase Ameliorates Cisplatin-Induced Nephropathy in Mice
Laboratory studyOther animalsHumans
- Design
- Laboratory study
- Subjects
- Male wild-type and Faah knockout C57BL6 mice given a single 30 mg/kg intraperitoneal dose of cisplatin; two human head and neck cancer cell lines
- Dose used in the study
- No palmitoylethanolamide was given; kidney PEA and OEA levels were measured
- Duration
- 72 hours after cisplatin
- What was measured
- Blood urea nitrogen, plasma creatinine, kidney injury markers and tubular damage; PEA and OEA tone; NF-kappa-B activity, p53, p21, IL-1 beta and immune cell infiltration; cisplatin anti-tumour effect in cancer cells with a FAAH inhibitor.
What the authors reported
Faah knockout mice had less cisplatin kidney injury than wild-type mice, with higher PEA and OEA, lower NF-kappa-B activity, DNA damage markers and IL-1 beta, and less macrophage and leukocyte infiltration. A FAAH inhibitor (PF-04457845) did not reduce cisplatin's anti-tumour effect in HN30 and HN12 cells.
Limits of this study
A mouse and cell study; it cannot show effect in people or animals treated in practice. PEA was raised by gene deletion, not given. Funding and conflicts not stated in the abstract.
Source
PubMed 36702548 · doi:10.1124/molpharm.122.000618
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.