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作 者:熊锦文[1] 胡廉[2] 官黄涛[2] 赵玉梅[1] 徐红[1] 于建萍[1] 熊承良[2]
机构地区:[1]武警湖北总队医院妇科,武汉市430061 [2]华中科技大学同济医学院计划生育研究所,武汉市430030
出 处:《医学分子生物学杂志》2013年第1期58-62,共5页Journal of Medical Molecular Biology
摘 要:目的研究鼠巨细胞病毒(MCMV)感染对雄鼠睾丸生殖细胞凋亡的影响,探讨睾丸组织核因子-κB亚基p65亲和肽(NF-κBp65)表达与生殖细胞凋亡的相关性。方法建立小鼠睾丸MCMV感染模型,设立实验组与对照组,分别于感染不同时段(小鼠一个生精周期内),采用Hoechst33258染色法对小鼠睾丸组织生精小管及间质细胞进行凋亡检测,采用免疫组织化学sP法检测小鼠睾丸组织内NF-κB065的表达。结果睾丸间质细胞的凋亡率在MCMV感染的第1天开始增多(P〈0.05),第4-6天达到高峰。第21天、第38天恢复正常。生精小管管周肌样上皮细胞的凋亡数在感染的第1天开始增多(P〈0.05).第6—9天达到高峰(P〈0.001),第21天、第38天也恢复正常。生精细胞的凋亡数在感染的第2天显著增加(P〈0.05),第6天达到高峰(P〈0.001);第14天起逐渐恢复正常。睾丸组织中NF-κBp65表达在MCMV感染第2天起开始增加(P〈0.05),感染的第6—9天增至高峰(P〈0.001),随感染时间延长逐渐下降,第21~28天恢复正常。结论MCMV急性感染可诱导睾丸生殖细胞凋亡,其凋亡程度与睾丸组织NF-κBp65表达呈正相关。提示NF-κBp65参与并调控了MCMV感染所致的生殖细胞凋亡,这可能是MC-MV感染的致病机制及机体抵御MCMV感染机制之一。Objective To study the effect of MCMV infection on the apoptosis of reproductive cells in male mice and the relationship between NF-κB p65 expression in testes and reproductive cell apoptosis after MCMV infection. Methods Murine testicular MCMV infection models were estab- lished and experiment and control groups designed in terms of different periods of MCMV infection (within one seminiferous cycle) . The apoptosis of seminiferous tubule and interstitial cells in mouse testicular tissues was detected by Hoechst33258 staining. The immunohistochemical SP method was used to determine the expression level of NF-κB p65 in testicular tissue. Results The apoptosis rate of interstitial cells began to increase on the first day of MCMV infection ( D1 ) ( P 〈 0.05 ), reached a peak on D4 to D6 (P 〈 0. 001 ) , and returned to normal on D21 and D38. The number of apoptot- ic peritubular myoid ceils in the convoluted seminiferous tubules was increased on D1 (P 〈0. 05), reached the peak on D6 to D9 (P 〈 0. 001 ), and also returned to normal on D21 and D38. The number of apoptotic seminiferous cells were significantly enhanced on D2 ( P 〈 0. 05 ), peaked on D6 ( P 〈 0. 001 ), and returned to normal on D14. The expression of NF-κB p65 protein in testiculartissues was increased since D2 ( P 〈 0. 05) , and reached a peak on D6 to D9 (P 〈 0. 001 ) . As in- fection continued, the expression of NF-κB p65 was decreased and returned to normal on D2I and D38 (P 〉0.05) . Conclusion Acute MCMV infection could induce the apoptosis of reproductive cells of the male mice. There was a positive correlation between the apoptotic degree and the NF-κB p65 expression. It was suggested that NF-κB p65 is implicated in the reproductive cell apoptosis after MCMV infection, which may be a pathogenic mechanism of MCMV infection and a mechanism for self-defense to MCMV infection.
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