实验动物与比较医学 ›› 2014, Vol. 34 ›› Issue (3): 181-186.DOI: 10.3969/j.issn.1674-5817.2014.03.003

• 论著 • 上一篇    下一篇

低氧肺动脉高压大鼠蛋白激酶CβII蛋白表达及膜转位水平的变化

郭万金1, 施熠炜2, 张爱珍1, 杜永成1   

  1. 1.山西医科大学 附属人民医院呼吸科, 太原 030001;
    2.第一医院呼吸科, 太原 030001
  • 收稿日期:2013-10-18 出版日期:2014-06-25 发布日期:2014-06-25
  • 作者简介:郭万金(1987-), 男, 呼吸内科学硕士研究生, 研究方向: 肺血管疾病专业。E-mail:guowanjin2@126.com
  • 基金资助:
    山西省卫生厅科技攻关计划项目(No 2011028)

Changes of PKCβII Protein Expression and Membrane Translocation in Pulmonary Artery of Rats with Hypoxic Pulmonary Hypertension

GUO Wan-jin1, SHI Yi-wei2, ZHANG Ai-zhen1, DU Yong-cheng1   

  1. 1. Department of Respiratory Medicine, People's Hospital of Shan Xi Medical University, Taiyuan 030001, China;
    2. Department of Respiratory Medicine, the First Hospital of Shan Xi Medical University, Taiyuan 030001, China
  • Received:2013-10-18 Online:2014-06-25 Published:2014-06-25

摘要: 目的 建立慢性低氧性肺动脉高压大鼠模型并初步探讨蛋白基酶CβII(PKCβII)在慢性低氧性肺动脉高压的发生发展过程中所起的作用。方法 建立慢性常压低氧肺动脉高压大鼠模型,将清洁级SD大鼠, 随机分为正常对照组、低氧1 d、3 d、7 d、14 d和21 d组,检测大鼠右心室收缩压(right ventricle systolic pressure, RVSP)和右心室肥厚指数(right ventricle hypertrophy index,RVHI),采用HE染色观察肺动脉病理学改变, Western blotting方法检测大鼠肺动脉内PKCβII蛋白表达和膜转位水平的变化。结果 (1)与正常对照组相比,低氧暴露1 d、3 d、7 d、14 d、21 d后RVSP均明显上升(P<0.05); RVHI低氧3 d、7 d、14 d、21 d组较正常对照组明显上升(P<0.05); 低氧暴露3、7和21 d组肺动脉病理学改变明显。(2)PKCβII蛋白的表达量在慢性低氧3 d、7 d、14 d和21 d与正常对照组相比明显降低(P<0.05),慢性低氧3 d后PKCβII膜转位水平较正常对照组明显下降(P<0.05)。结论 PKCβII蛋白表达和膜转位水平的下调可能参与了大鼠慢性低氧性肺动脉高压的发生和发展过程。

关键词: 蛋白激酶CβII, 慢性低氧, 肺动脉高压, 膜转位, 蛋白表达

Abstract: Objective To establish rats model of chronic pulmonary hypertension (PH) and preliminarily explore the effect of PKCâII in the development of hypoxia-induced pulmonary hypertension. Methods Male SD rats were exposed to normobaric hypoxia to induce PH model. The rats were randomly divided into six groups, and exposed to normoxia control and to normoxia hypoxia for 1 d, 3 d, 7 d, 14 d and 21 d. Right ventricle systolic pressure (RVSP) and right ventricle hypertrophy index(RVHI) were measured. Pathological changes of the pulmonary arteries were observed by HE staining. The changes of PKCβII protein expression and membrane translocation in pulmonary arteries were also detected by Western blotting. Results RVSP increased significantly after hypoxic exposure for 1 d, 3 d, 7 d, 14 d and 21 d when compared with the normoxia control(P<0.05); There were significant rise in RVHI after hypoxic exposure for 3 d, 7 d, 14 d and 21 d (P<0.05). The pathological changes of the pulmonary arteries were significant at 3 d, 7 d, 21 d. PKCâII protein expression decreased significantly at 3 d, 7 d, 14 d, 21 d after chronic hypoxia than those of normal control groups respectively(P<0.05). Significant decrease of PKCβII membrane translocation level in pulmonary arteries of rats could be detected after hypoxic exposure 3 d(P<0.05). Conclusion The decrease in protein expression and membrane translocation of PKCβII may be involved in the development of the chronic hypoxia-induced pulmonary hypertension.

Key words: Protein kinase CβII, Chronic hypoxia, Pulmonary hypertension, Membrane translocation, Protein expression

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