RESUMEN
The aim of this study was to investigate the role of T-helper cell (Th)1/Th2 cytokines in the chronicity of hepatitis C virus (HCV) infection and the outcome of interferon (IFN) alpha therapy. A total of 30 patients with chronic hepatitis C were enrolled in the study. The levels of Th1/Th2 cytokines were determined. The differentiation of HCV genotypes was determined by direct sequencing. HCV RNA loads were detected by fluorescence quantitative polymerase chain reaction (qPCR). In chronic hepatitis C, the levels of interleukin (IL)-2 and transforming growth factor (TGF)-ß significantly decreased, and IL-5 and IL-18 levels increased compared with normal controls. The IL-6 serum levels were directly proportional to the serum levels of alanine aminotransferase, and were inversely proportional to the HCV RNA loading levels. Patients with severe hepatitis C had higher levels of IL-4, IL-6, and IL-1ß compared to milder cases. Patients with genotype 1 showed higher serum levels of IL-6 than those with genotype 2. The levels of IL-2 and IL-18 showed a decreasing tendency, whereas TGF-ß, IL-6, and IL-1ß showed an increasing tendency over time. There was no difference in any cytokines detected between the response and nonresponse groups before IFN therapy. However, the IFN-y level increased after IFN therapy in the response group. There was no correlation between the Th1/Th2 cytokine levels in the serum before IFN treatment and in the outcome of IFN therapy. Increasing IFN-y levels in the serum induced by IFN treatment is associated with systemic vascular resistance.
Asunto(s)
Antivirales/uso terapéutico , Hepacivirus/efectos de los fármacos , Hepatitis C Crónica/tratamiento farmacológico , Hepatitis C Crónica/patología , Interferón-alfa/uso terapéutico , Polietilenglicoles/uso terapéutico , Balance Th1 - Th2/efectos de los fármacos , Adulto , Alanina Transaminasa/sangre , Alanina Transaminasa/genética , Femenino , Expresión Génica/efectos de los fármacos , Genotipo , Hepacivirus/fisiología , Hepatitis C Crónica/sangre , Hepatitis C Crónica/virología , Humanos , Interferón alfa-2 , Interferón gamma/sangre , Interferón gamma/genética , Interleucina-18/sangre , Interleucina-18/genética , Interleucina-1beta/sangre , Interleucina-1beta/genética , Interleucina-2/sangre , Interleucina-2/genética , Interleucina-4/sangre , Interleucina-4/genética , Interleucina-5/sangre , Interleucina-5/genética , Interleucina-6/sangre , Interleucina-6/genética , Masculino , Persona de Mediana Edad , Proteínas Recombinantes/uso terapéutico , Células TH1/efectos de los fármacos , Células TH1/virología , Células Th2/efectos de los fármacos , Células Th2/virología , Factor de Crecimiento Transformador beta/sangre , Factor de Crecimiento Transformador beta/genética , Resultado del Tratamiento , Carga Viral/efectos de los fármacosRESUMEN
We examined microRNA-181b (miRNA) expression in prostate cancer tissues and its effect on the prostate cancer cell line PC-3. Tissues from 27 cases of prostate cancer and 30 samples of normal human prostate were collected by surgical removal. Total miRNA was extracted, and the relative expression of miR-181b was quantified using RT-PCR. miR-181b ASO was transfected into prostate cancer PC-3 cells. miR-181b expression in transfected and non-transfected cells was measured using RT-PCR. Changes in cell apoptosis were measured using flow cytometry. MTT and cell growth curve methods were used to assess the influence of miR-181b expression on cell proliferation. The changes in cell invasive ability in vitro were detected using the Transwell chamber method. miR-181b was up-regulated in the prostate cancer tissues compared with the normal prostate samples. It was down-regulated after miR-181b ASO transfection into the prostate cancer PC-3 cells. Down-regulation of miR-181b in the PC-3 cell induced apoptosis, inhibited proliferation, and depressed invasion of PC-3 cells in vitro. As miR-181b is over-expressed in prostate cancer, its down-regulation could have potential as gene therapy for prostate cancer by inducing apoptosis, inhibiting proliferation and depressing invasion by cancer cells.