Dietary sphingomyelin inhibits colonic tumorigenesis with an up-regulation of alkaline sphingomyelinase expression in ICR mice.
Anticancer Res
; 28(6A): 3631-5, 2008.
Article
en En
| MEDLINE
| ID: mdl-19189644
ABSTRACT
BACKGROUND:
Sphingomyelin (SM) hydrolysis generates biologically active products regulating cell growth, differentiation and apoptosis. Dietary SM has been found to inhibit colonic tumorigenesis. Alkaline sphingomyelinase (alk-SMase) is the key enzyme responsible for sphingomyelin digestion in the gut. Whether or not dietary sphingomyelin affects alk-SMase expression was examined in a colon cancer animal model. MATERIALS ANDMETHODS:
Imprinting control region (ICR) mice were injected with 1,2-dimethylhydrazine (DMH) and then fed a diet with or without SM (0.5 g/kg in diet) for 22 weeks. The colonic tumorigenesis and alk-SMase activity were determined and alk-SMase expression was examined by Western blot and PCR.RESULTS:
Dietary SM inhibited the tumorigenesis and increased the alk-SMase activity in the colon by 65%. The increased activity was associated with increased enzyme protein and mRNA expression. No changes of acid and neutral sphingomyelinase activities were found.CONCLUSION:
Long-term supplementation with dietary sphingomyelin up-regulates colonic alk-SMase expression, which may contribute to the inhibitory effects of sphingomyelin against colonic carcinogenesis.
Buscar en Google
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Esfingomielina Fosfodiesterasa
/
Esfingomielinas
/
Neoplasias del Colon
Límite:
Animals
Idioma:
En
Revista:
Anticancer Res
Año:
2008
Tipo del documento:
Article
País de afiliación:
China