RESUMO
Sex-linked dwarf (SLD) chickens have been widely used in cross breeding of broilers and laying hens. To study the molecular mechanisms underlying growth hormone receptor (GHR) in SLD chickens, the expression profiles of GHR were measured in three growth related tissues (liver, breast, and thigh) in male and female S2 SLD chickens at seven growth stages (1 day, 3 weeks, 7 weeks, 9 weeks, 11 weeks, 13 weeks, and 15 weeks). Growth curves of body weight were fitted using logistic and Gompertz models. The results show that the inflexion week and inflexion weight in male chickens was earlier than in female chickens. Regarding the expression profiles of GHR, there was no significant difference between tissues at hatching. The expression peaked at 7 weeks and dropped by degrees in muscle tissue; hepatic expression increased with age and was positively correlated with body weight. Taken together, these results would provide a basis for further study on the molecular mechanisms underlying GHR regulation in SLD chickens.
Assuntos
Cruzamento , Galinhas/crescimento & desenvolvimento , Galinhas/genética , Regulação da Expressão Gênica no Desenvolvimento , Receptores da Somatotropina/genética , Animais , Feminino , Modelos Logísticos , Masculino , Dinâmica não Linear , Especificidade de Órgãos/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores da Somatotropina/metabolismo , Aumento de Peso/genéticaRESUMO
We evaluated the cytotoxicity of 1-dodecyl-3-methylimidazo-lium bromide ([C12mim][Br]) on HepG2 cells and its influence on plasma membrane permeability. The results showed that [C12mim][Br] inhibited HepG2 cell growth and decreased cell viability in a concentration-depen-dent manner. The results also revealed that [C12mim][Br] exposure induced apoptosis in [C12mim][Br]-treated HepG2 cells. In addition, the results showed that [C12mim][Br] increased membrane permeability in HepG2 cells. These results suggest that plasma membrane permeability may be responsible for apoptosis induced by [C12mim][Br] in HepG2 cells.