摘要
目的:研究细胞外信号调节蛋白激酶1/2(ERK1/2)通路在雄激素缺乏引起的勃起功能障碍(ED)中的作用。方法:8周龄健康雄性SD大鼠30只,随机分成对照组(A组)、去势组(B组)、去势后补充雄激素组(C组)。B组和C组大鼠均手术去势,其中C组大鼠在去势1周后注射十一酸睾酮(TU)100 mg/kg,其余组则注射等量生理盐水。1个月后测各组大鼠血清睾酮浓度、平均颈动脉压(MAP)、阴茎海绵体内压(ICP),通过Western印迹检测大鼠阴茎海绵体ERK1/2、内皮型一氧化氮合酶(e NOS)的蛋白表达。结果:B组大鼠血清睾酮[(1.27±0.48)nmol/L]较A组[(17.14±1.07)nmol/L]和C组[(16.24±1.90)nmol/L]明显降低(P<0.05),ICP/MAP比值B组较A组和C组明显下降(P<0.05);Western印迹结果显示ERK1/2在各组中表达基本一致(P>0.05),而磷酸化细胞外信号调节蛋白激酶1/2(P-ERK1/2)在B组中表达高于A组和C组(P<0.05),e NOS在B组中表达明显低于A组和C组(P<0.05)。结论:雄激素可能通过调控ERK1/2通路改善去势大鼠的勃起功能。
Objective： To investigate the role of the extracellular signal-regulated protein kinase 1/2 （ERK1/2） pathway in erectile dysfunction （ED） caused by the absence of testosterone （T）. Methods： We randomly divided 30 eight-week-old healthy male SD rats into groups A （control）, B （castration）, and C （castration ＋ androgen replacement）. The rats in groups B and C were castrated surgically, and those in C injected with T undecanoate （ 100 mg/kg） at 1 week after castration, while the others with 0.9% normal saline instead. At 1 month after treatment, we determined the serum T level, intracavernous pressure （ICP）, and mean carotid arterial pressure （MAP） of the rats, and detected the expressions of ERK1/2 and endothelial nitric oxide synthase （eNOS） by Western blot. Results ： The serum T level was significantly lower in group B （ [ 1.27 ± 0.48 ] nmol/L） than in A （ [ 17.14 ±1.07 ] nmol/L） and C （ [ 16.24 ± 1.90 ] nmol/L） （ P 〈 0. 05 ）, and so were ICP and MAP （P 〈 0.05 ）. The expression of ERK1/2 showed no statistically significant differences among the three groups （P 〉 0.05 ）. , that of phosphatase ERK1/2 was markedly higher while that of eNOS remarkably lower in group B than in A and C （ both P 〈 0.05 ）. Conclusion ： Androgen replacement may improve the erectile function of castrated rats by regulating the ERK1/2 pathway.
出处
《中华男科学杂志》
CAS
CSCD
北大核心
2015年第11期967-972,共6页
National Journal of Andrology
基金
国家自然科学基金(81200435)~~
