中国比较医学杂志2012，Vol.22Issue(9)：26-30,40,后插2,7.DOI:10.3969.j.issn.1671.7856.2012.009.006
慢性低氧所致肺动脉高压对大鼠肺血管平滑肌细胞及成纤维细胞中蛋白激酶CβI的膜转位和蛋白表达量的影响
Determination of PKCβI Membrane Translocation and Protein Expression in Pulmonary Artery Smooth Muscle Cells and Fibroblasts of Rats with Chronic Hypoxia-induced Pulmonary Hypertension
程振玲 1于文燕 1聂欣 1施熠炜 2杜永成1
作者信息
- 1. 山西医科大学附属人民医院呼吸科,太原030001
- 2. 山西医科大学第一临床医学院呼吸科,太原030001
- 折叠
摘要
Abstract
Objective By observing the influence of PKCβI membrane translocation and protein expression level in pulmonary artery Smooth muscle cells and Fibroblasts of chronic hypoxia-induced rat pulmonary hypertension, discuss the function of PKCβI in process of chronic hypoxia-induced rat pulmonary hypertension preliminary. Methods Chronic atmospheric pressure hypoxic PH model rats were established. Male SD rats were randomLy divided into six groups, and exposed to normoxia control or to normoxia hypoxia for ld,3d,7d,14d and 21 d to induce pulmonary hypertension. Western blot and immunohistochemistry were used to detect the expression of PKCβI membrane translocation and protein expression level in pulmonary artery Smooth muscle cells and Fibroblasts of chronic hypoxia-induced rat pulmonary hypertension. Results (1) RVSP and RV/(LV + S) increased significantly than normal control groups ( P < 0. 05 ) , rats pulmonary vascular obvious thickening after chronic hypoxia 3d,7d,14d and 21 d. (2). PKCβI was expressed in rat pulmonary artery Smooth muscle cells and Fibroblasts, and its protein expressions decreased at 14d after chronic hypoxia than normal control groups(P<0.05 ). Conclusions PKCβI protein expression is involved in the development of pulmonary vascular remodeling of chronic hypoxia-induced rat PH.
关键词
PKCβI/慢性低氧/肺动脉高压/膜转位/蛋白表达水平Key words
Protein kinase C βI (PKC βI )/ Chronic hypoxia/ Pulmonary hypertension (PH)/ Membrane translocation/ Protein expression分类
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程振玲,于文燕,聂欣,施熠炜,杜永成..慢性低氧所致肺动脉高压对大鼠肺血管平滑肌细胞及成纤维细胞中蛋白激酶CβI的膜转位和蛋白表达量的影响[J].中国比较医学杂志,2012,22(9):26-30,40,后插2,7.
