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首页> 中文期刊> 《中国病理生理杂志》 >Rho激酶在糖尿病血管内皮功能改变中的作用

Rho激酶在糖尿病血管内皮功能改变中的作用

         
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摘要

AIM; To invesligale the role of Rho kinase in diabelic vascular endothelial dysfunction. METHODS; SD rats, genelic db/db diabelic model and high - fat diel - induced obese mice were used in ihis study. The thoracic aorta of the rals or mice were isolaled and suspended in organ balh or myograph for measuremenl of the changes in isometric tensions. The levels of phosphorylaled endolhelial nilric oxide synlhase(eNOS) were determined by Weslern blolling. Throm-boxane B2(TXB2) , proslaglandin F2α(PGF2α) and thromboxane receplor (TP receplor) aclivalors in artery were measured by ELISA. RESULTS; Endolhelium - dependenl vasorelaxalion [ Emax was (78. 8 ±10.6)% in conlrol group] was allenualed by TP receplor aclivalion [Emax was (17. 9 ±5. 1)% in Rho kinase aclivalion group] , which was ameliorated by Rho kinase inhibilors [ Emax was (62. 0 ± 11. 2) % in Rho kinase inhibilion group]. The improved endolhelium - dependenl vasorelaxalion by inhibilion of Rho kinase was abolished by prelrealmenl wilh the inhibilor of eNOS. Consistently, the level of phosphorylaled eNOS was inhibited by TP receplor aclivalion, which was reversed by inhibilion of Rho kinase. The endolhelium - dependenl vasorelaxalion was also improved by Rho kinase inhibilors in diabelic and obese animals. The levels of TXB2 and PGF2α in the arteries were increased in diabelic animals compared wilh the controls. CONCLUSION; Rho kinase plays a role in diabelic endothelial dysfunclion, which may be related lo TP receptor aclivalion and eNOS inhibilion.%目的:探讨Rho激酶激活在糖尿病血管内皮功能损伤中的作用.方法:利用正常SD大鼠、基因型糖尿病动物模型和高脂饮食诱发的小鼠肥胖模型,用器官浴槽和肌动描记方法对血管功能进行检测,用免疫印迹方法对血管组织中内皮型一氧化氮合酶(eNOS)磷酸化水平进行测定,用ELISA方法对血管组织中血栓烷受体(TP受体)激活物进行测量.结果:TP 受体激活可以抑制正常血管的内皮依赖性舒张,使最大舒张值(Emax)由正常组的(78.8±10.6)% 降到 (17.9±5.1)%; Rho激酶抑制剂预处理翻转了TP受体的抑制作用,Emax值为 (62.0±11.2)%;抑制eNOS抵消了Rho激酶抑制剂对血管功能的改善作用.与此相一致,TP受体激活可以抑制正常血管eNOS磷酸化水平,并且该作用被Rho激酶抑制剂所翻转.此外,抑制Rho激酶可以使糖尿病小鼠和肥胖小鼠的血管内皮依赖性舒张作用得到改善,Emax值显著增加.并且,与对照组相比,糖尿病动物血管组织中血栓烷B2和前列腺素F2α水平升高.结论:Rho激酶参与了糖尿病血管内皮功能紊乱的调节,可能与TP受体激活和抑制eNOS活性有关.

著录项

  • 来源
    《中国病理生理杂志》 |2012年第6期|1103-1108|共6页
  • 作者

    吴健美; 刘传飞; 刘翠清; 陈晓娜; 郭正祥; 纪晓微; 施巧雅; 尹洪萍; 沈礼; 汝海龙; 林国华;

  • 作者单位

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

    杭州师范大学基础医学部生理教研室,浙江,杭州,310036;

  • 原文格式 PDF
  • 正文语种 chi
  • 中图分类 血液循环;
  • 关键词

    Rho激酶; 受体,血栓烷; 内皮,血管; 糖尿病;

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