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作 者:蔡卫平[1] 聂静敏[1] 刘金峰[1] 许敏[1] 胡凤玉[1] 李凌华[1] 唐小平[1]
出 处:《中华传染病杂志》2012年第12期727-730,共4页Chinese Journal of Infectious Diseases
基 金:基金资助:国家重大科技项目“艾滋病和病毒性肝炎等重大传染病防治”科技重大专项资助项目(2012ZXl0001003-003);广东省自然科学基金资助项目(10451006002006054,S2011010005587)
摘 要:目的探讨慢性丙型肝炎患者外周血单个核细胞(PBMC)中载脂蛋白BmRNA编辑酶催化多肽样蛋白3G(APOBEC3G)mRNA表达水平及外源性IFN对APOBEC3GmRNA表达的影响。方法以28例慢性丙型肝炎患者为病例组、14名健康人为对照组,用TaqMan适时定量PCR方法检测PBMC中APOBEC3GmRNA的表达水平(为相对表达水平,即与管家基因18srRNA表达水平的比值);动态观察慢性丙型肝炎患者IFN治疗前、治疗后2、4、12、24、36和48周时PBMC中APOBEC3GmRNA水平的变化,并同步用ELISA方法检测血浆中IFN-α含量。采用SPSS11.0分析软件对收集的数据进行t检验和重复测量资料的方差分析。结果病例组治疗前APOBEC3GmRNA表达水平为1.60×10-4±1.35×10-4,较健康对照组(6.20×10-4±1.30×10-4)显著降低(t=3.147,P=0.003);IFN治疗后,APCIBEC3GmRNA表达显著上调,治疗12、24、36和48周时分别达到5.69×10-3±1.61×10-2、1.01×10-2土2.15×10、2.01×10-2±3.75×10-2.45×10-2±4.08×10-2,显著高于治疗前水平(F值分别为3.46、5.67、10.27、25.65,P值分别为0.042、0.030、0.010、0)。血浆IFN—α含量也随治疗上升,在2周升至较高水平并维持至观察结束。结论HCV感染可能是APOBEC3G表达下调的原因之一。Objective To study the mRNA expression of apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) in the peripheral blood mononuclear cells (PBMC) in patients with chronic hepatitis C (CHC) and its regulation by exogenous interferon-α (IFN-α). Methods Twenty-eight CHC patients were recruited as case group and 14 healthy subjects were recruited as control group. APOBEC3G mRNA level (the ratio of APOBEC3G mRNA to housekeep gene 18s rRNA) in PBMC was determined by TaqMan real-time polymerase chain reaction (RT- PCR). APOBEC3G mRNA levels were also dynamically measured in CHC patients treated with pegylated interferon (IFN)-α 2a at week 0, 2, 4, 12, 24, 36 and 48 of treatment, and the plasma levels of IFN-α were simultaneously detected by enzyme-linked immunosorbent assay (ELISA). Thedata were analyzed by t test and analysis of variance using SPSS 11.0 software. Results The level of APOBEC3G mRNA in PBMC of CHC patients before treatment was 1.60 × 10-4 -+- 1.35 × 10-4 , which was significantly lower than healthy controls 6.20× 10-4 ±1. 30× 10-4 (t=3. 147, P=O. 003). The expressions of APOBEC3G mRNA were upregulated at week 12, 24, 36 and 48 of IFN treatment, which were 5.69×10-a±1.61×10-2, 1.01×10 2±2. 15×10 -2, 2.01×10-2±3.75×10 2 and 2.45× 10-2 and 2.45.08×10-2 , respectively, and all higher than that of pretreatment (F= 3.46, 5. 67, 10.27 and 25.65, respectively; P=0. 042, 0. 030, 0. 010 and 0, respectively). IFN-a level in plasma were increased with treatment and reached the plateau at week 2 of the treatment until the end o{ observation. Conclusion Hepatitis C virus infection may be one of the reasons of APOBEC3G downregulation.
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