摘要
目的通过观察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(PKCβI)的膜转位和蛋白表达量的影响,初步探讨PKCβI在慢性低氧诱导大鼠肺动脉高压的发生、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,将雄性SD大鼠随机分为正常对照组、低氧1 d、3 d、7d、14 d和21 d组,应用蛋白免疫印迹和免疫组化技术检测肺动脉高压形成过程中大鼠肺血管平滑肌细胞及成纤维细胞中PKCβI的膜转位和蛋白表达水平。结果 (1)RVSP和RV/(LV+S)比值较正常对照组明显增加(P<0.05),低氧后3 d、7 d、14 d和21 d后大鼠肺血管明显增厚;(2)大鼠肺血管平滑肌细胞和成纤维细胞均有PKCβI的表达,且低氧14 d后PKCβI的蛋白表达量较正常对照组相比降低(P<0.05)。结论 PKCβI蛋白表达量的下调可能参与了慢性低氧诱导的大鼠肺动脉高压肺血管重塑的发生、发展过程。
Objective By observing the influence of PKCβ1 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 1 d ,3d,Td, 14d and 21d to induce pulmonary hypertension. Western blot and immunohistochemistry were used to detect the expression of PKCβI membrane transloeation 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 pulmonaryvascular obvious thickening after chronic hypoxia 3d,7d, 14d and 21d. （2）. PKCβI was expressed in rat pulmonary artery Smooth musele eells and Fibroblasts, and its protein expressions decreased at 14d after ehronic bypoxia 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.
出处
《中国比较医学杂志》
CAS
2012年第9期26-30,40,I0002,共7页
Chinese Journal of Comparative Medicine
关键词
PKCβI
慢性低氧
肺动脉高压
膜转位
蛋白表达水平
Protein kinase C βI （PKC βI ）
Chronic hypoxia
Pulmonary hypertension （PH）
Membrane translocation
Protein expression
