中文摘要：

目的通过研究灭活HIV-1ⅢB颗粒对人结肠癌HT-29细胞的增殖、凋亡和紧密连接的影响，探讨HIV-1病毒子在“AIDS肠道病灶论”中的直接作用机制。方法将AT-2灭活的HIV-1ⅢB 颗粒加入到HT-29培养系统中,使p24抗原终质量浓度为1ng／ml；WST-1法检测HT-29的增殖率；运用流式细胞术检测HT-29中Ki-67和Apo2．7的表达以及线粒体膜电势和线粒体质量的变化；运用流式细胞术检测HT-29紧密连接蛋白Occludin的表达。结果灭活HTV-1ⅢB抑制HT-29增殖并抑制Ki-67表达；灭活HIV-1mn诱导HT-29凋亡并降低线粒体膜电势和线粒体质量；灭活HIV-1ⅢB下调Occludin表达，提示其破坏细胞的紧密连接。结论AT-2灭活HIV-1ⅢB能够抑制HT-29增殖，诱导HT-29凋亡，并破坏HT-29紧密连接，提示在“AIDS肠道病灶论”中，导致肠黏膜屏障完整性受损的因素除了HIV-1引发的“旁观者效应”外，HIV-1病毒子本身可以对肠上皮细胞（intestinaleDitheliaIcell，IEC）产生细胞毒作用；而肠黏膜通透性增加会引起肠菌转位，继而引发系统性免疫过度活化。

英文摘要：

This study was conducted to explore the effects of AT-2-inactivated HIV-1 particles on the proliferation, apoptosis and tight junction of HT-29 cells. HIV-1ⅢB particles were inactivated by AT-2 chemical and then added to HT-29 culture system in optimal concentration. The proliferation and Ki-67 expression of HT- 29 was evaluated by WST-1 assay and flow cytometry, respectively. The apoptosis of HT-29 was evaluated by Apo2.7 staining, as well as DIOC6（3） and NAO staining. Meanwhile, the tight junction of HT-29 was assessed by Occludin staining. Data showed that the proliferation of HT-29 was inhibited by AT-2-inactivated HIV-1ⅢB particles. In addition, AT-2-inactivated HIV-1ⅢBparticles induced HT-29 apoptosis, and disrupted the tight junction of HT-29. The results indicated that AT-2-inactivated HIV-1ⅢB particles strikingly affected the proliferation, apoptosis and tight junction of HT-29 cells, which means besides its immunopathogenicity, the eytopathogenicity of HIV-1 virion contributes to the intestinal pathogenesis of AIDS. The increased intestinal permeability might result in gut bacteria transloeation, which then triggers systemic immune hyperactivation.