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作 者:石裕明[1] 张立煌[2] 孙永良[2] 方海林[2] 何南祥[2] 刘克洲[2] 李敏伟[2] 姚航平[2] 吴婉芬[1]
机构地区:[1]广州市第八人民医院传染病研究所,510060 [2]浙江医科大学传染病研究所
出 处:《中华实验和临床病毒学杂志》1999年第3期269-273,共5页Chinese Journal of Experimental and Clinical Virology
摘 要:目的 了解白介素(IL)4 对重型病毒性肝炎患者外周血单个核细胞(PBMCs) 中肿瘤坏死因子(TNF)α和IL1αmRNA的表达的影响。方法 TNFα和IL1αmRNA的表达水平采用半定量逆转录聚合酶链反应(RTPCR) 进行检测。结果 IL4 均以剂量依赖的方式抑制治疗前、后亚急性重型肝炎患者PBMCs TNFα和IL1αmRNA的表达,在发病初期,IL4 于1 000Uml 时接近最大抑制效应;而恢复期患者,IL4 于100Uml 时即接近最大抑制效应,剂量- 反应曲线明显左移。如以100Uml 的IL4 处理PBMCs,恢复期亚急性重型肝炎患者PBMCs TNFα和IL1αmRNA的抑制率接近50% 。另外还发现,在发病初期,IL4 对内毒素血症和HBeAg 阳性患者PBMCsTNFα和IL1αmRNA表达的抑制作用低于阴性的患者。结论 IL4 对发病初期患者PBMCTNFα和IL1αmRNA 表达的抑制作用明显低于恢复期患者。Objective The aim of this study was to compare the influence of IL 4 on the expression of TNF α and IL 1α mRNA by PBMCs from patients with subfulminant viral hepatitis(SFH) before and after IL 4 treatment. Methods The expression levels of TNF α and IL 1α mRNA by PBMCs were assessed by semiquantitative RT PCR.Results IL 4 suppressed the expression of both TNF α and IL 1 αmRNA by PBMCs from SFH patients before and after treatment dose dependently. However, their dose response curves showed significant differences. The inhibitory effect could be observed at a concentration of 100U/ml and was near to maximum at 1 000U/ml in acute phase, whereas the same suppressive action of IL 4 was reached at 100U/ml in recovery phase. When PBMCs were cultured in the presence of IL 4 at a concentration of 100U/ml, IL 4 down regulated the production of both TNF α and IL 1α mRNA by acute phase PBMCs only to 18.18~21.98% of control cells(in absence of IL 4), while the inhibitory rates were all near to 50% in recovery phases. Moreover, it was also found that the suppressive effect of IL 4 on the expression of PBMCs TNF α and IL 1α mRNA in the patients with endotoxinemia and HBeAg was significantly decreased in acute phase.Conclusions The inhibitory effect of IL 4 on the expression of PBMCs TNF α and IL 1α mRNA is markedly decreased in acute phase as compared with that in recovery phase and this declined response may be related to endotoxinemia and viremia.
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