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目的探讨高脂及糖尿病性勃起功能障碍大鼠阴茎海绵体中内皮型一氧化氮合酶(eNOS)和内皮素-1(ET-1)蛋白表达的变化及其可能的机制。方法 58只SPF级雄性SD大鼠随机分成3组:(1)对照组(n=14),普通饲料喂养;(2)高脂组(n=15),高脂饲料喂养24周后在原饲料配方中加入含0.2%硫氧嘧啶继续喂养;(3)糖尿病组(n=29),高脂饲料喂养24周后腹腔注射20mg/kg STZ;于实验开始后36周末,检测大鼠血糖、血清总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、胰岛素水平;成模后用阿朴吗啡诱导并观察大鼠阴茎勃起功能变化;采用Western blot检测大鼠阴茎海绵体组织eNOS和ET-1蛋白表达。结果血糖、胰岛素、血脂检测结果显示成功建立了高脂和糖尿病模型。与对照组相比,高脂及糖尿病组大鼠勃起功能明显下降,eNOS蛋白表达显著降低,而ET-1显著升高(P<0.05);与高脂组相比,糖尿病组eNOS与ET-1表达进一步失衡,且阴茎勃起功能障碍较高脂组加重。结论糖尿病和高脂血症导致勃起功能障碍的发病机制可能与阴茎海绵体组织内eNOS和ET-1表达失衡密切相关。
Objective To investigate the changes of the expression of endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) in the corpus cavernosum of hyperlipidemic and diabetic erectile dysfunction rats and its possible mechanism. Methods Fifty-eight SPF male Sprague-Dawley rats were randomly divided into three groups: (1) control group (n = 14) fed with normal diet; (2) fed with high fat diet (n = 15) (3) In diabetic group (n = 29), high-fat diet was injected intraperitoneally 20mg / kg STZ 24 weeks after the beginning of the experiment. At the end of the experiment 36 weeks after the start of the experiment, blood glucose, serum (TC), triglyceride (TG), LDL-C, HDL-C and insulin were measured. After modeling, apomorphine was used to induce and observe the rats Penile erectile dysfunction; Western blot was used to detect the expression of eNOS and ET-1 in the penis of corpus cavernosum. Results Blood glucose, insulin, blood lipid test results showed that the model of hyperlipidemia and diabetes was established successfully. Compared with the control group, the erectile function and the expression of eNOS protein were significantly decreased and the ET-1 level was significantly increased in the HF and DM groups (P <0.05). Compared with the hyperlipidemia group, eNOS and ET- 1 expression further imbalance, and erectile dysfunction than the high-fat group increased. Conclusion The pathogenesis of erectile dysfunction caused by diabetes and hyperlipidemia may be closely related to the imbalance of eNOS and ET-1 expression in corpus cavernosum.