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作 者:李海仙[1] 曾耀英[1] 肇静娴[1] 曾祥凤[1] 李孝建[1]
机构地区:[1]暨南大学组织移植与免疫教育部重点实验室,广州510632
出 处:《中国免疫学杂志》2006年第5期445-448,共4页Chinese Journal of Immunology
基 金:国家自然科学基金面上项目(30500466);广东省自然科学基金博士启动项目(5300419)
摘 要:目的:研究相当于妊娠后外周血和胎盘局部浓度的孕酮(P4)体外对HIV-1感染及复制的影响。方法:检测终浓度为10-6mol/L(相当于妊娠妇女外周血水平)和10-5mol/L(相当于母胎界面局部浓度)的P4对HIV-1介导细胞融合的影响;ELISA法检测感染HIV的MT-2细胞培养上清p24抗原含量来探讨对HIV-1复制的影响;流式细胞术检测对淋巴细胞活化后CD69表达的影响和3H-TdR掺入法检测对淋巴细胞增殖的影响。结果:10-5mol/L的P4可以明显抑制HIV-1介导的细胞融合,并且降低感染细胞培养上清中p24抗原含量,两种浓度对淋巴细胞的活化和增殖都有抑制作用。结论:相当于妊娠后母胎界面局部浓度的P4体外可以抑制HIV-1感染和复制,其机制与抑制淋巴细胞活化和增殖有关。Objective :To investigate the effects of progesterone( P4 ), corresponding to peripheral blood levels during pregnancy and the fetal-maternal interface, on HIV-1 infection and replication in vitro. Methods:P4 in final concentration of 10^-6 mol/L, corresponding peripheral blood levels during pregnancy, and 10^-5 mol/L detected at the fetal-maternal interface on HIV-1 infection and rephcation in vitro, which were detected by HIV-1 mediated cell fusion and p24 production monitored by ELISA respectively. The effects of P4 on activation and proliferation of lymphocytes were determined by detecting CD69 expression by multicolor flow cytometric analysis and the 3H-thymidine( [^3H]-TdR) incorporation. Results:P4 could dramatically inhibit formation of fusions mediated by HIV- 1 and decrease releasing of p24 in concentration of 10^-5 mol/L, and P4 could inhibit activation and proliferation of lymphocytes in given concentration. Conclusion:P4 in concentration of 10^-5 mol/L detected at the fetal-maternal interface can inhibit the infection and rephcation of HIV-1 in vitro, and the mechanism correlate to inhibiting effect on activation and proliferation of lymphocytes.
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