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作 者:刘凤霞[1] 腊博雅 刘琪[2] 艾热提·吾杰克 热西旦·亚力坤 彭世宇[2] 张盼盼[1] 马文静[1] 阿地力江·伊明[1]
机构地区:[1]新疆医科大学基础医学院人体解剖学教研室,乌鲁木齐830011 [2]新疆医科大学临床医学院
出 处:《中国男科学杂志》2016年第9期5-9,共5页Chinese Journal of Andrology
基 金:大学生创新性实验计划项目(20151076005);国家自然科学基金(81260581)
摘 要:目的研究RhoA、Rho激酶(ROCK1)在异常黏液质证候及阳痿病证大鼠模型阴茎组织中的表达,并探讨维药伊木萨克片干预后对其表达的影响。方法选用50只性功能正常的雄性SD大鼠,其中10只为正常对照组(N组),余40只为造模组,采用湿寒饲料+湿寒环境的干预条件建立异常黏液质证候模型大鼠,20周筛选出阳痿病证模型大鼠,并将其分为病证模型组(A1)和病证药物反证组(A3);未成阳痿的大鼠分为证候模型组(B1),证候药物反证组(B3)。伊木萨克片反证2周后,免疫组化和Western-blot方法检测各组大鼠阴茎组织中RhoA、ROCK1的表达。结果 A1、A3、B1组大鼠阴茎组织中RhoA、ROCK1表达均高于N组(P<0.05)。A3组大鼠阴茎组织中RhoA、ROCK1表达均低于A1组(P<0.05)。B3组大鼠阴茎组织中RhoA、ROCK1表达明显低于B1组(P<0.05)。结论 RhoA/ROCK1信号系统可以促进大鼠异常黏液质证候及阳痿病证的发生,伊木萨克片可能通过抑制RhoA/ROCK1信号通路对异常黏液质证候及阳痿病证大鼠模型发挥治疗作用。Objeotive To study the expression of RhoA/Rho-kinase in penis tussue of rat model with abnormal phlegmatic syndrome and impotence disease and intervention effect of Yimusake on it. Methods Total of 50 normal mature male SD rats were used in the study, and 10 of them were randomly chosen as the normal control group (N group), other 40 were treated with spinach and coriander diet in a cold and humid environment to have abnormal phlegmatic syndrome and impotence disease. The established rat models were randomly divided into abnormal phlegmatic syndrome group (/31), medication disproof group of abnormal phlegmatic syndrome (B3), impotence model group (A 1), medication disproof group of impotence model (A3). After 2 weeks Yimusake treatment, we measured the expression of RhoA/Rho-kinase in penis tissues of different groups. Results The results showed that RheA, ROCK1 expressions in A1, A3, B 1 group were higher than that in N group (P〈0.05). RhoA and ROCK1 expressions in A3 group were lower than that in A1 group (P〈0.05). RhoA and ROCK1 expressions in B3 group were lower than that in B1 group (P〈0.05). Conclusion RhoA/Rho kinase signaling system can contribute to the development of abnormal phlegmatic syndrome and impotence disease. Yimusake may have a therapeutic role for abnormal phlegmatic syndrome and impotence disease through inhibiting RhoA/Rho kinase signaling pathways.
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