RESUMEN
The increase in prevalence of asthma is strongly dependent on environmental factors, including foods. Significant decreases in the intake of dietary zinc may be an important contributing factor to the increasing incidence of asthma. As zinc can not passively diffuse across cell membranes, specific zinc transporters are required for zinc influx and efflux. There are two identified gene families involved in zinc homeostasis, ZnT transporters and ZIP transporters. In this study, we aimed to investigate the expression of these zinc transporters mRNA in the leukocytes of asthmatic infants. Asthmatic infants (n = 9) and healthy infants (n = 9) were included in this study. Five zinc transporters were chosen: ZnT-1, ZnT-3, ZnT-5, ZIP-1, and ZIP-2. Levels of zinc were determined in serum and expression of zinc transporters mRNA were measured. Serum zinc levels were significantly lower in asthmatic infants (P < 0.01); Expression of ZnT-1, ZnT-3, ZnT-5, ZIP-1 mRNA were not significantly different between two groups, but expression of ZIP-2 mRNA was significantly higher (P < 0.01) in the asthmatic group than the control group. In conclusion, overexpression of ZIP-2 mRNA was found in the leukocytes of asthmatic infants.
Asunto(s)
Asma/metabolismo , Proteínas de Transporte de Catión/metabolismo , Leucocitos/metabolismo , ARN Mensajero/metabolismo , Proteínas Portadoras/genética , Proteínas Portadoras/metabolismo , Proteínas de Transporte de Catión/genética , Preescolar , Femenino , Humanos , Lactante , Masculino , Zinc/sangreRESUMEN
AIM: To elucidate effects and mechanisms of emodin in prostate cancer cells. METHODS: Viability of emodin-treated LNCaP cells and PC-3 cells was measured by MTT assay. Following emodin treatments, DNA fragmentation was assayed by agarose gel electrophoresis. Apoptosis rate and the expression of Fas and FasL were assayed by flow cytometric analysis. The mRNA expression levels of androgen receptor (AR), prostate-specific antigen (PSA), p53, p21, Bcl-2, Bax, caspase-3, -8, -9 and Fas were detected by RT-PCR, and the protein expression levels of AR, p53 and p21 were detected by Western blot analysis. RESULTS: In contrast to PC-3, emodin caused a marked increase in apoptosis and a decrease in cell proliferation in LNCaP cells. The expression of AR and PSA was decreased and the expression of p53 and p21 was increased as the emodin concentrations were increased. In the same time, emodin induced apoptosis of LNCaP cells through the upregulation of caspase-3 and -9, as well as the increase of Bax /Bcl-2 ratio. However, it did not involve modulation of Fas or caspase-8 protein expression. CONCLUSION: In prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.
