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目的建立泌乳素瘤性勃起功能障碍大鼠模型(P-ED),研究过氧化物酶体增殖因子活化受体(PPAR-γ)配体罗格列酮对泌乳素瘤性勃起功能障碍大鼠阴茎神经型一氧化氮合酶(nNOS)表达的影响。方法雄性Wistar大鼠腹腔内注射乙烯雌酚(DES)建立泌乳素瘤模型。8周后进行阿扑吗啡(APO)试验,筛选出阴茎勃起功能障碍(ED)模型后,分为对照组、泌乳素瘤ED模型组、罗格列酮治疗组,免疫组化方法测定大鼠阴茎组织nNOS表达水平的变化。结果与对照组相比,注射DES 8周时大鼠阴茎勃起次数显著减少。12周时阴茎组织nNOS表达减少。罗格列酮治疗4周后血清PRL水平明显降低,阴茎组织nNOS表达增加。结论阴茎组织nNOS表达减少可能是泌乳素瘤大鼠发生ED的主要机制。罗格列酮能降低泌乳素瘤ED大鼠的PRL水平,改善阴茎勃起功能,增加阴茎nNOS表达。
Objective To establish a prolactinoma-induced erectile dysfunction rat model (P-ED) and investigate the effect of rosiglitazone, a ligand of peroxisome proliferator activated receptor (PPAR-γ), on the development of prolactinoma-induced erectile dysfunction Effect of penile neuronal nitric oxide synthase (nNOS) expression. Methods Male Wistar rats were injected intraperitoneally with diethylstilbestrol (DES) to establish a prolactinoma model. Eight weeks later, apomorphine (APO) test was performed to screen the model of erectile dysfunction (ED). The rats were divided into control group, ED model group, rosiglitazone treatment group and immunohistochemistry Changes of nNOS expression in penile tissue. Results Compared with the control group, the number of penile erections in rats after 8 weeks of DES injection was significantly reduced. Penile tissue nNOS expression decreased at 12 weeks. After 4 weeks of rosiglitazone treatment, serum PRL levels were significantly decreased and nNOS expression in penile tissues increased. Conclusion The decrease of nNOS expression in penile tissue may be the main mechanism of ED in prolactinoma rats. Rosiglitazone can reduce PRL levels in prolactinoma ED rats, improve penile erection, and increase penile nNOS expression.