RESUMO
This study examined the effects of road transportation on metabolic and immunological responses in dairy heifers. Twenty Holstein heifers in early pregnancy were divided into non-transported (NT; n = 7) and transported (T; n = 13) groups. Blood was collected before transportation (BT), immediately after transportation for 100 km (T1) and 200 km (T2), and 24 h after transportation (AT). The T heifers had higher (P < 0.05) blood cortisol and non-esterified fatty acid concentrations after T1 and T2 than did NT heifers. By contrast, the T heifers had lower (P < 0.05) serum triglyceride concentrations after T1 and T2 than had the NT heifers. The serum cortisol and triglyceride concentrations returned (P > 0.05) to the BT concentrations at 24 h AT in the T heifers. The granulocyte-to-lymphocyte ratio and the percentage of monocytes were higher (P < 0.05) after T2 in the T heifers than in the NT heifers, suggesting that transportation stress increased the numbers of innate immune cells. T heifers had higher (P < 0.01) plasma haptoglobin concentrations than NT heifers 24 h AT. In conclusion, transportation increased cortisol secretion and was correlated with increased metabolic responses and up-regulation of peripheral innate immune cells in dairy heifers.
Assuntos
Bovinos/imunologia , Bovinos/metabolismo , Hidrocortisona/metabolismo , Imunidade Inata/imunologia , Estresse Fisiológico/imunologia , Estresse Fisiológico/fisiologia , Meios de Transporte , Animais , Feminino , Granulócitos/imunologia , Haptoglobinas/metabolismo , Hidrocortisona/sangue , Linfócitos/imunologia , Gravidez , Fatores de Tempo , Triglicerídeos/sangueRESUMO
Ginsenosides, the major active component of ginseng, are traditionally used to treat various diseases, including cancer, inflammation, and obesity. Among these, compound K (CK), an intestinal bacterial metabolite of the ginsenosides Rb1, Rb2, and Rc from Bacteroides JY-6, is reported to inhibit cancer cell growth by inducing cell-cycle arrest or cell death, including apoptosis and necrosis. However, the precise effect of CK on breast cancer cells remains unclear. MCF-7 cells were treated with CK (0-70 micrometer) for 24 or 48 h. Cell proliferation and death were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Changes in downstream signaling molecules involved in cell death, including glycogen synthase kinase 3ß (GSK3ß), GSK3ß, ß-catenin, and cyclin D1, were analyzed by western blot assay. To block GSK3ß signaling, MCF-7 cells were pretreated with GSK3ß inhibitors 1 h prior to CK treatment. Cell death and the expression of ß-catenin and cyclin D1 were then examined. CK dose- and time-dependently inhibited MCF-7 cell proliferation. Interestingly, CK induced programmed necrosis, but not apoptosis, via the GSK3ß signaling pathway in MCF-7 cells. CK inhibited GSK3ß phosphorylation, thereby suppressing the expression of ß-catenin and cyclin D1. Our results suggest that CK induces programmed necrosis in MCF-7 breast cancer cells via the GSK3ß signaling pathway.
Assuntos
Morte Celular/efeitos dos fármacos , Ginsenosídeos/metabolismo , Quinase 3 da Glicogênio Sintase/metabolismo , Western Blotting , Proliferação de Células/efeitos dos fármacos , Feminino , Citometria de Fluxo , Formazans/análise , Glicogênio Sintase Quinase 3 beta , Humanos , Células MCF-7 , Coloração e Rotulagem , Sais de Tetrazólio/análiseRESUMO
In the present study, we examined the effects of ginsenoside Re (Re) on cytokine expression, cytokine-dependent autophagy and cell survival in human CD4(+) T cells. When CD4(+) T cells isolated from human peripheral blood were treated with Re, LC3 and monodansylcadaverine (MDC), representative markers of autophagy, were decreased in a dose-dependent manner. Interestingly, Re suppressed the production of interferon-gamma (IFN-gamma) and immunity-related GTPase family M (IRGM) in CD4(+) T cells whereas no changes in other autophagy-related signaling molecules (ERK, p38 and AKT-mTOR-p70S6k) were found. Concomitantly, we observed that Re increased the proliferation of CD4(+) T cells with decreased cell death. Our results demonstrate that ginsenoside Re enhanced viability of CD4(+) T cells through the regulation of IFN-gamma-dependent autophagy activity.