论文部分内容阅读
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。
AIM: To investigate the role of the extracellular signal-regulated protein kinase 1/2 (ERK1 / 2) pathway in androgen deficiency-induced erectile dysfunction (ED). Methods: Thirty male Sprague-Dawley rats, 8 weeks old, were randomly divided into control group (A group), castration group (B group) and androgen administration group (C group) after castration. Rats in group B and group C were surgically cast. Rats in group C were injected with 100 mg / kg of testosterone undecanoate (TU) one week after castration, and the other groups received normal saline. After 1 month, serum testosterone concentration, mean carotid artery pressure (MAP) and intracavernosal pressure (ICP) were measured. Western blotting was used to detect the expression of ERK1 / 2 and endothelial nitric oxide synthase e NOS) protein expression. Results: Serum testosterone levels in group B were significantly lower than those in group A [(17.14 ± 1.07) nmol / L and [16.24 ± 1.90] nmol / L] (P <0.05). Western blotting results showed that the expression of ERK1 / 2 in each group was basically the same (P> 0.05), while the ratio of phosphorylated extracellular signal-regulated protein The expression of P-ERK1 / 2 in group B was higher than that in group A and C (P <0.05). The expression of eNOS in group B was significantly lower than that in group A and C (P <0.05). Conclusion: Androgens may improve erectile function in ovariectomized rats by regulating ERK1 / 2 pathway.