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作 者:肖凡[1,2] 乔雍[1,2] 张仁雯[1,2] 常路丝[1,2] 成军[1,2] 魏红山[1,2]
机构地区:[1]首都医科大学附属北京地坛医院传染病研究所 [2]新发突发传染病研究北京市重点实验室,北京100015
出 处:《中华实验和临床感染病杂志(电子版)》2013年第4期11-13,共3页Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition)
基 金:国家自然科学基金(No.30872243;81071411;30901273)
摘 要:目的探讨抑制O-糖基化修饰对乙型肝炎病毒颗粒组装的影响。方法采用O-糖基化修饰抑制剂Benzyl-α-GalNAc干预HepG2.2.15细胞。经7-AAD染色,应用流式细胞仪检测细胞凋亡情况。采用实时荧光定量PCR方法检测上清HBV病毒载量。应用酶联免疫吸附试验(ELISA)检测上清乙型肝炎病毒大蛋白(the hepatitis B virus large surface protein,HBV LHBs)水平。采用蛋白免疫印迹(Western blot)方法检测细胞中LHBs蛋白含量。结果 Benzyl-α-GalNAc能显著促进细胞凋亡,上清中HBV DNA和LHBs水平呈剂量依赖性增加;Benzyl-α-GalNAc抑制细胞中LHBs蛋白表达。结论抑制细胞O-糖基化修饰促进细胞凋亡,从而释放HBV LHBs和病毒颗粒;但在某种程度上抑制细胞O-糖基化修饰能够抑制细胞内LHBs合成。Objective To investigate the effect of the inhibition of O-glycosylation on HBV assembly. Methods HepG2.2.15 cells treated with O-glycosylation inhibitor, Benzyl-α-GalNAc, were dyed with 7-AAD and examined by FACS for cell apoptosis. HBV DNA loading in cell supernatant was determined by real-time PCR. HBV LHBs levels in cell supernatant was tested by ELISA. LHBs levels in cells was analyzed by Western blot. Results Benzyl-α-GalNAc could signiifcantly induce cell apoptosis. HBV DNA and LHBs levels in cell supernatant were increased in a dose dependent manner. However, Benzyl-α-GalNAc inhibited LHBs synthesis. Conclusions Inhibition of O-glycosylation could induce cell apoptosis and release HBV LHBs and virus. In some extent, inhibition of O-glycosylation may inhibit LHBs synthesis.
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