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机构地区:[1]南京医科大学附属南京第一医院泌尿外科,江苏南京210006 [2]上海交通大学附属上海市第一人民医院泌尿外科,上海200086
出 处:《中华男科学杂志》2007年第2期110-113,共4页National Journal of Andrology
基 金:国家自然科学基金(30440060)
摘 要:目的:研究前列腺不同区带间细胞的增殖和凋亡,并比较其差异。方法:应用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测17例正常前列腺移行带和外周带、20例良性前列腺增生(BPH)移行带上皮细胞凋亡率,免疫组化法检测细胞增殖核抗原(PCNA)及Bcl-2表达。RT-PCR法半定量验证Bcl-2 mRNA表达。结果:①正常前列腺移行带上皮细胞凋亡率和增殖率均显著低于外周带[(13.7±4.32%)vs(20.9±6.44)%和(14.6±4.34)%vs(25.6±6.35)%,P<0.01],增生的移行带上皮细胞凋亡减少,同时细胞增殖增加。②正常前列腺外周带上皮细胞Bcl-2表达率低于移行带,后者又显著低于BPH移行带(P<0.01)。增生的移行带中Bcl-2表达率与上皮细胞凋亡率呈显著负相关(rs=-0.867,P<0.01)。结论:移行带和外周带存在细胞增殖和凋亡率差异。增生的移行带上皮细胞凋亡减少,同时细胞增殖增加,这可能是BPH的重要病理基础。Bcl-2在移行带高表达参与了BPH病理过程。Objective: To determine and compare the difference of cell apoptosis and proliferation in the transition and peripheral zones in the human prostate. Methods: Seventeen normal prostate glands from organ donors were sampled from normal men according to McNeal's zonal anatomy, and 20 hyperplastic transition zones obtained from prostatectomy specimens of BPH patients. Cell proliferation and Bcl-2 expression were assessed by immunostaining using PCNA and anti-Bcl-2 antibodies, while apoptotic bodies were specifically stained using TUNEL. Bcl-2 mRNA expression was detected by RT-PCR. Results: In the normal epithelium, the rates of cell proliferation and apoptosis were markedly decreased in the transition zone as compared with the peripheral zone. The proliferation index was significantly increased in the hyperplastic transition zone in BPH, while the apoptosis index significantly decreased in comparison with the normal prostate. Bcl-2 was significantly greater in the normal transition epithelium than in the peripheral zone, and over-expressed in the hyperplastic transition zone. There was a significant negative correlation between the Bcl-2 expression and the apoptosis of the epithelial cells in the hyperplastic transition zone( r = - 0.867, P 〈 0.01 ). Conclusion : The hyperplastic transition zone may result from both an increase of cell proliferation and a failure of cell apoptosis process by blocking cell apoptosis. Nail J Androl,2007,13( 2 ) :110-113
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