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Research for erectile dysfunction by DNA microarray assay and PWV/PVM

DNA 微阵列检测和 PWV/PVM 对勃起功能障碍的研究

基本信息

批准号：
18591781
负责人：
NISHIMATSU Hiroaki
金额：
$ 2.44万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

Erectile dysfunction is mainly due to the inability of the cavernosal smooth muscle of the penis to undergo complete relaxation. In the aging rat model, erectile dysfunction is accompanied by a reduction of penile smooth muscle compliance and, in very old animals, by a decrease in penile nitric oxide synthase (NOS), which is responsible for the synthesis of the mediator of penile erection, nitric oxide (NO).we examined alterations in penile gene expression in diabetic rats and littermate controls. With the use of Affymetrix GeneChip arrays and statistical filtering. Athelosclerosis related genes cause vascular endothelial dysfunction and is a major risk factor for cardiovascular diseases. The data from this study are relevant to understanding the mechanisms underlying the pathophysiological effect of microcirculation disorder, particularly on endothelial function and pathogenesis of atherosclerosis. CYP3A correlated information about inactivating action of estrogen/testosterone has close relationship with erectile dysfunction and LOH conditions. The data suggest that a significant inverse relation exists between presumed atherosclerotic load (as assessed by the number of erectile dysfunction risk factors and events) and aortic compliance determined noninvasively based on aortic pulse wave velocity measurements. Erectile dysfunction risk shows outward symptom during the early stage of cardiovascular risk factors. If these findings are confirmed by prospective, longitudinal follow-up studies, such measurements may prove useful as a noninvasive marker of vascular risk.

勃起功能障碍主要是由于阴茎海绵体平滑肌不能完全松弛。在老龄大鼠模型中，勃起功能障碍伴随着阴茎平滑肌顺应性的降低，在非常老的动物中，伴随着阴茎一氧化氮合酶（NOS）的降低，NOS负责合成阴茎勃起的介质一氧化氮（NO）。我们研究了糖尿病大鼠和同窝对照组阴茎基因表达的改变。使用Affyssin基因芯片阵列和统计过滤。血管内皮功能障碍是心血管疾病的主要危险因素。本研究的结果有助于深入了解微循环障碍的病理生理学作用机制，特别是微循环障碍对内皮功能的影响和动脉粥样硬化的发病机制。CYP 3A相关的雌激素/睾酮失活作用信息与勃起功能障碍和洛性丢失密切相关。这些数据表明，一个显着的负相关关系之间存在假定动脉粥样硬化负荷（评估勃起功能障碍的危险因素和事件的数量）和主动脉顺应性确定的主动脉脉搏波速度测量的基础上非侵入性。勃起功能障碍风险在心血管危险因素的早期表现为外在症状。如果这些发现被前瞻性纵向随访研究证实，这些测量可能被证明是有用的血管风险的非侵入性标志物。