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作 者:李瑞 刘康 李浩 张岩 陈智[1] 袁彗星 李明超 王涛[1] 蓝儒竹[1] 刘继红[1] 饶可 Li Rui;Liu Kang;Li Hao;Zhang Yan;Chen Zhi;Yuan Huixing;Li Mingchao;Wang Tao;Lan Ruzhu;Liu Jihong;Rao Ke(Department of Urology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430030,China)
机构地区:[1]华中科技大学同济医学院附属同济医院泌尿外科,武汉430030
出 处:《中国男科学杂志》2018年第5期3-8,共6页Chinese Journal of Andrology
基 金:国家自然科学基金(81200435)
摘 要:目的研究代谢综合征导致勃起功能障碍大鼠阴茎海绵体组织中氧化应激变化,探讨氧化应激导致代谢综合征大鼠勃起功能障碍的机制。方法将40只3周龄雄性SD大鼠随机分为实验组30只(高脂高糖饲料喂养6个月)和正常对照组10只(普通饲料喂养6个月)。喂养6个月后检测实验组和正常对照组大鼠体质量、血脂、空腹血糖、血压和胰岛素水平,筛选出代谢综合征大鼠,随后阿扑吗啡试验筛选出代谢综合征相关的勃起功能障碍(MED)大鼠。检测喂养后MED组和正常对照组大鼠阴茎海绵体内压(ICP)/平均动脉压(MAP)变化,应用Westernblot检测两组大鼠阴茎海绵体组织中NADPH氧化酶各亚基和eNOS表达,DHE染色检测阴茎海绵体组织活性氧水平,ELISA检测阴茎海绵体组织中cGMP浓度。结果 (1)喂养后MED组大鼠体质量、空腹血糖、血浆中胰岛素和胆固醇水平较正常对照组明显升高(均P <0.05);(2)喂养后MED组大鼠Max ICP/MAP较正常对照组明显降低(P <0.05);(3)喂养后MED组大鼠阴茎海绵体组织中gp91phox蛋白表达和活性氧水平较正常对照组明显升高(均P <0.05);(4)喂养后MED组大鼠阴茎海绵体组织中eNOS蛋白表达和cGMP浓度较正常对照组明显降低(均P<0.05)。结论氧化应激可能通过引起阴茎海绵体内皮细胞功能障碍从而导致代谢综合征大鼠勃起功能障碍的发生。Objective To investigate the role of oxidative stress in erectile dysfunction of penile corpus caversum smooth muscles of metabolic syndrome rats and its molecular mechanism. Methods Forty male Sprague Dawley rats with three-week-old were randomly divided into control and experimental groups. Rats in the control group(n=10) were fed on a regular diet for 6 months and those in the experimental group(n=30) on a high-fat and high glucose diet for the same period of time. Afterwards, body weight, blood pressure, plasma insulin, fasting blood glucose levels and plasma lipids were assessed. An apomorphine test was conducted to confirm metabolic syndrome related erectile dysfunction(MED). Erectile responses were evaluated by determining the mean arterial blood pressure(MAP) and intracavernosal pressure(ICP). Levels of protein expression were examined by western blotting. Level of reactive oxygen species was examined by DHE staining. ELISA was used to detect the concentration of cyclic guanosine monophosphate(cGMP). Results Body weight, fasting blood glucose, plasma insulin and plasma total cholesterol were increased in MED rats compared with those in control rats(each P <0.05). Maximum ICP/MAP and the concentration of cGMP were significantly decreased in MED rats(each P <0.05). The expression of eNOS was downregulated in MED rats and the expressions of gp91 phox and reactive oxygen species(ROS) were upregulated in MED rats(each P < 0.05). Conclusion Oxidative stress may be involved in the MED in rats.
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