PPARgamma Ligand-Induced Decrease of in vivo Tumor Growth Accompanied by Increased Cytolytic Activity of Splenocytes
Korean Journal of Pathology
;
: 7-14, 2007.
Artículo
en Inglés
| WPRIM
| ID: wpr-71842
ABSTRACT
BACKGROUND:
Recent studies have proposed the use of peroxisome proliferator activated receptor-gamma (PPARgamma) ligands as new chemotherapeutic agents for human malignant tumors. However the in vivo mechanism of PPARgamma ligands on cellular toxicity is not clear. Therefore we examined the anti-tumor effects of the PPARgamma ligand, rosiglitazone (ROS), in animal models.METHODS:
To evaluate the effect of RSO on splenocytes, an in vitro and in vivo study was performed. Cytolytic activity was measured by use of a 51Cr release assay. The splenic natural killer (NK) cell population and effector-target conjugation were measured by flow cytometric analysis.RESULTS:
In 9L glioma bearing rats, 30 mg/kg/d of ROS treatment induced a significant decrease of subcutaneous tumor growth accompanied by an increased cytolytic activity of splenocytes and of the splenic NKR-P1bright/CD3- NK cell population. In normal rats, systemic administration of ROS also increased the cytolytic activity of splenocytes, the splenic NK cell population, and effector-target conjugation. Moreover, we found that a concentration of 20micrometer ROS caused an increase in the cytolytic activity of splenocytes, and a concentration of 50micrometer ROS increased effector-target conjugation in vitro.CONCLUSIONS:
These results suggest that increased splenic cytolytic activity and NK cell population may contribute to the anti-tumor effects of PPARgamma ligands in vivo. However, the roles of NK cells in the PPARgamma ligand-induced anti-tumor activity should be further investigated.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Bazo
/
Células Asesinas Naturales
/
Peroxisomas
/
Modelos Animales
/
PPAR gamma
/
Glioma
/
Ligandos
Límite:
Animales
/
Humanos
Idioma:
Inglés
Revista:
Korean Journal of Pathology
Año:
2007
Tipo del documento:
Artículo
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