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- W46270571 abstract "1409 Objectives: The peroxisome proliferator-activated receptor-γ (PPAR-γ) is a member of the nuclear receptor superfamily of ligand-dependent transcription factors. And diclofenac β-dimethyl-aminoethanol is non-steroidal anti-inflammatory drugs (NSAIDs) to treat colic and inflammatory diseases. PPAR-γ agonists (Rosiglitazone) have been demonstrated to inhibit many cytokines in macrophage and have anti-inflammatory effect. The aim of this study is to demonstrate the variation of glucose uptake in macrophage and tumor cells when these drugs were added. Methods: Cell uptake studies were carried out in RAW264.7 (macrophage cell line) and KB (nasopharyngeal carcinoma cell line), A549 (lung adenocarcinoma cell line) cells using 18F-FDG. And we performed western blotting experiment to ascertain the expression of glucose transporter and hexokinase. Results: Cell uptake studies showed different result between rosiglitazone and diclofenac. 18F-FDG uptake by diclofenac was decreased about 40~50% in macrophage and tumor cells. The expression of proteins related FDG uptake such as GLUT1, GLUT3 and hexokinase showed well corresponded result with cell uptake in macrophages. The result of 18F-FDG uptake by rosiglitazone was not changed in RAW264.7 and significantly increased in tumor cells. These results also corresponded with those of western data. Conclusions: In conclusion, we demonstrated the role of PPAR-γ agonist and NSAIDs on 18F-FDG uptake in macrophages and various tumor cells. Futhermore these results might be used to differentiate between tumors and inflammatory lesions on 18F-FDG scan." @default.
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- W46270571 date "2007-05-01" @default.
- W46270571 modified "2023-09-27" @default.
- W46270571 title "The effect of PPAR-γ and NSAIDs on 18F-FDG uptake in the macrophage and tumor cells" @default.
- W46270571 hasPublicationYear "2007" @default.
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