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作 者:李靖宇[1] 李永智[1] 李子政[1] 张西玲[1] 刘屹立[1]
机构地区:[1]中国医科大学附属第四医院泌尿外科,沈阳110032
出 处:《中国男科学杂志》2013年第10期15-19,共5页Chinese Journal of Andrology
基 金:辽宁省教育厅课题编号201202251
摘 要:目的:研究在Ⅱ型糖尿病影响下,细胞外信号调节激酶(ERK)在前列腺组织中的表达,探讨Ⅱ型糖尿病易伴发良性前列腺增生的机制。方法选取10周龄雄性SD大鼠造模,分别造成糖尿病合并前列腺增生组、糖尿病组、前列腺增生组,另外设正常对照组。应用免疫组织化学及Western blot方法检测ERK1/2及P-ERK1/2在的前列腺组织中的表达情况,计算ERK1/2磷酸化活化程度。结果免疫组化结果显示:ERK1/2在各组间的表达无明显差别,差异无统计学意义(P>0.05),P-ERK1/2在糖尿病合并前列腺增生组中的表达呈强阳性,而在糖尿病组与前列腺增生组中的表达以阳性结果为主,实验对照组中表达以阴性为主;Western blot结果可以看出ERK1/2在各组间表达无明显差别,差异无统计学意义(P>0.05);而P-ERK1/2在各组中的表达不同,在糖尿病合并前列腺增生组中的表达最强,在实验对照组中表达甚微,差异有统计学意义(P<0.01),而在糖尿病组及前列腺增生组中的表达有差别(P>0.05)。结论推测ERK是Ⅱ型糖尿病及良性前列腺增生的发病机制之一,ERK的高磷酸化程度是造成两种疾病高伴发率的原因之一。Objective To study the expression and activation of ERK in the prostate tissueunder influence of the typeⅡ diabetes mellitus, and explore the mechanism of typeⅡ diabetes mellitus frequently causing benign prostatic hyperplasia. Methods Ten-weeks old male SD rats were induced into diabetes mellitus and prostate hyperplasia rat models(Group1), diabetes mellitus rat models (Group2), prostatic hyperplasia rat model(Group3) and the control. The expressions of ERK1/2 and P-ERK1/2 in the prostate tissues were detected by IHC and western blot, respectively.Results IHC results showed that there was no significant difference in ERK1/2 expression among these groups (P〉0.05), the expression of the P-ERK1/2 was notable upregulated in the diabetes mellitus and prostate hyperplasia rat model group, whereas slightly upregulated in the diabetes mellitus group and prostatic hyperplasia group, as compared with that of the control. Western blot results also demonstrated that there was no significant difference in ERK1/2 among these groups (P〉0.05), but the expression of the P-ERK1/2 was diverse in groups, the highest expression was in the diabetes mellitus and prostate hyperplasia group, and little expression in the control group, the difference was statistical significance (P〈0.01), the expression of P-ERK1/2 was obvious difference between in diabetes mellitus group and in prostate Hyperplasia group (P〉0.05).Conclusion It was conjectured that the ERK might be one of the pathogenetic mechanisms of typeⅡ diabetes mellitus and benign prostatic hyperplasia. The high level of ERK phosphorylation might be one reason of the two kinds of disease with a high intercurrent rate.
关 键 词:糖尿病 2型 前列腺增生 细胞外信号调节MAP激酶类 大鼠
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