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机构地区:[1]四川省自贡市第四人民医院泌尿外科,自贡643000 [2]重庆医科大学附属第二医院泌尿外科
出 处:《中国男科学杂志》2012年第12期3-7,共5页Chinese Journal of Andrology
摘 要:目的探讨5α还原酶抑制剂对人前列腺增生组织中IGF-1、PCNA、Caspase3的影响及相关性。方法采用免疫组化法(PV9000法)检测良性前列腺增生患者服5α还原酶抑制剂组(简称服药组)与未服药组IGF-1及PCNA、Caspase3的表达,并分析三者间的相关性。结果(1)前列腺增生患者服药组IGF-1阳性表达率及PCNA表达较未服药组表达明显减弱(P〈0.05),Caspase3阳性率表达在服药组明显增加(P〈0.05)。服药组尿道周IGF-1和PCNA的表达强于包膜下部位的趋势,而Caspase3弱于包膜下,但差异均无统计学意义(P〉0.05)。(2)5α还原酶抑制剂作用下IGF-1,PCNA和CaSPase3的相关性表达研究显示,IGF-1与PCNA呈正相关(JP〈0.01),IGF-1与Caspase3的表达呈负相关(P〈0.05)。结论(1)5α还原酶抑制剂与IGF-1密切相关,可能通过抑制IGF-1途径抑制细胞增殖和促进凋亡。(2)5α还原酶抑制剂对前列腺增生包膜下及尿道周抑制作用存在差异,可能是不能完全抑制前列腺细胞增生和促进凋亡的原因。Objective To investigate the effects of 5 a -reductase inhibitor on the expressions of IGF-l(insulin -like factor-1), PCNA(proliferation cell nuclear antigen) and Caspase3 in human prostatic hyperplastic tissues and its relationship. Methods The expressions ofPCNA, Caspase3, IGF-1 were detected by immunohistochemical analysis in prostate tissues of BPH patients treated with 5α -reductase inhibitor.and the relationships among PCNA, Caspase3, IGF-1 were analyzied. Results (1) The positive rate of IGF-1 and PCNA in the treated group with 5α -reductase inhibitor were markedly lower than those of the untreated group (P〈0.05). There was significant difference in the positive rate of Caspase3 in two groups.The tendency of IGF-1 and PCNA in periurethal tissues higher than those of under amicula in treated BPH group was discovered,Caspase3 lower than those of under amicula, but there was no statistically significant. (2) There was a positive correlation between IGF-1 and PCNA(P〈0.01).On the contrary, the expression of IGF-1 was negatively correlated with the expression of Caspase3 in the treated group(P〈0.05). Conclusion (1)5 a -reductase inhibitor might reduce cell proliferation and enhance cell apoptosis by inhibiting the expression of IGF-1 ; (2)A difference was found in inhibition effect on different BPH sites by 5 a -reductase inhibitor,which was probably associated with incompletely inhibition of prostatic cell proliferation and cell apoptosis increase.
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