Early-stage Type 2 Diabetes Mellitus Impairs Erectile Function and Neurite Outgrowth From the Major Pelvic Ganglion and Downregulates the Gene Expression of Neurotrophic Factors
详细信息    查看全文
文摘
To assess neurite sprouting and gene expression of neurotrophic factors, nerve markers, and apoptosis in the major pelvic ganglia (MPGs) of rats with type 2 diabetes mellitus (T2DM) as it relates to erectile function.Materials and MethodsMale rats were fed high-fat diet for 2 weeks followed by 2 low-dose injections of streptozotocin (20 mg/kg). In 3 groups (controls, 3-week, or 5-week T2DM), erectile function was measured by ratios of intracavernosal pressure to mean arterial pressure after cavernous nerve stimulation. MPGs were harvested, and gene expressions of neurotrophic factor 3, nerve growth factor, glial cell line-derived neurotrophic factor, brain-derived neurotrophic factor, caspase-1, -3, -9, beta tubulin type III, and neuronal nitric oxide synthase were quantified by quantitative polymerase chain reaction. Additional MPGs were harvested and cultured in Matrigel. Neurite outgrowth from the MPG was evaluated at 48 hours after culture.ResultsErectile function was significantly decreased in all rats with T2DM. Gene expressions of neurotrophic factor 3, nerve growth factor, glial cell line-derived neurotrophic factor, and brain-derived neurotrophic factor were slightly lower at 3 weeks and significantly lower at 5 weeks after T2DM induction. Gene expression of apoptotic markers caspase-1, -3, -9, and neuronal markers beta tubulin type III and neuronal nitric oxide synthase remained unchanged. Rats with T2DM had shorter neurite length and less neurite sprouting than did the control MPG.ConclusionEarly-stage T2DM downregulates neurotrophic factors, induces erectile dysfunction, and impairs MPG neurite outgrowth, suggesting that erectile dysfunction may be prevented by supplementing neurotrophic factors at early-stage T2DM.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700