CAJ | 학술논문

目的通过观察慢性低氧所致肺动脉高压对大鼠肺动脉内蛋白激酶Cα(PKCα)的膜转位和蛋白表达量的影响,初步探讨PKCα在慢性低氧诱导大鼠肺动脉高压的发生和发展过程中所起的作用.方法采用慢性常压低氧[氧浓度(10±0.1)％]大鼠肺动脉高压模型,将雄性SD大鼠随机分为正常对照组、低氧1d、3d、7d、14 d和21d组,检测大鼠右心室收缩压(RVSP)和右心室肥厚指数(RVHI),肺组织苏木精-伊红(HE)染色,应用蛋白免疫印迹和免疫组织化学的方法检测PKCα膜转位和蛋白表达水平的变化.结果 ①低氧1d、3d、7d、14 d和21d组与正常对照组相比,RVSP和RV/(LV+S)比值均明显增加(P＜0.05),低氧暴露3d、7d、14 d和21 d后大鼠肺动脉壁明显增厚;②PKCα的蛋白表达量在慢性低氧1d、3d、7d和14 d后比正常对照组明显下降(P＜0.05).结论 PKCα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的发生和发展过程.
목적 통과관찰만성저양소치폐동맥고압대대서폐동맥내단백격매Cα(PKCα)적막전위화단백표체량적영향,초보탐토PKCα재만성저양유도대서폐동맥고압적발생화발전과정중소기적작용.방법 채용만성상압저양[양농도(10±0.1)％]대서폐동맥고압모형,장웅성SD대서수궤분위정상대조조、저양1d、3d、7d、14 d화21d조,검측대서우심실수축압(RVSP)화우심실비후지수(RVHI),폐조직소목정-이홍(HE)염색,응용단백면역인적화면역조직화학적방법검측PKCα막전위화단백표체수평적변화.결과 ①저양1d、3d、7d、14 d화21d조여정상대조조상비,RVSP화RV/(LV+S)비치균명현증가(P＜0.05),저양폭로3d、7d、14 d화21 d후대서폐동맥벽명현증후;②PKCα적단백표체량재만성저양1d、3d、7d화14 d후비정상대조조명현하강(P＜0.05).결론 PKCα단백표체량적하조가능삼여료만성저양유도적대서폐동맥고압적발생화발전과정.
Objective To investigate the changes of PKCα membrane translocation and protein expression levels in pulmonary arteries of hypoxia-induced pulmonary hypertension of rats,and therefore to explore the effect of PKCα in the development of hypoxia-induced pulmonary hypertension.Methods Male SD rats were randomly divided into six groups,and exposed to normoxia control or to normoxia hypoxia [(10 ± 0.1)％ oxygen] for 1,3,7,14 and 21 days to induced pulmonary hypertension.Right ventricle systolic pressure (RVSP) and right ventricle hypertrophy index (RVHI) were measured.Pulmonary tissues of rats were stained by hematoxylin-eosin (HE).The changes of PKCα membrane translocation and protein expression levels in pulmonary arteries were determined by using Western blot and Immunohistochemical stain.Results RVSP and RVHI weight ratio increased significantly under hypoxic exposures when compared with the normoxia control (P＜0.05).The pulmonary vascular walls of rats are obviously thickening after hypoxic exposure for 3,7,14 and 21 days.The protein expression levels of PKCα in pulmonary arteries decreased significantly at 1,3,7 and 14 days after hypoxic exposures when compared with that of normoxia control group (P ＜0.05).Conclusions The decrease of protein expression level of PKCα in pulmonary arteries may be involved in the development of hypoxia-induced rats pulmonary hypertension.