低氧大鼠肺动脉内皮细胞VEGF变化与PKC活性关系的探讨  

THE RELATIONSHIP BETWEEN VEGF LEVEL AND PKC ACTIVITY IN PULMONARY ARTERIAL VASCULAR ENDOTHELIAL CELLS OF RAT DURING HYPOXIA

作　　者：杨曦明[1] 谢印芝[1] 聂鸿靖[1] 尹昭云[1] 

机构地区：[1]军事医学科学院卫生学环境医学研究所,天津300050

出　　处：《中国应用生理学杂志》2000年第3期250-253,共4页Chinese Journal of Applied Physiology

基　　金：国家自然科学基金!资助项目 (39730 190 )

摘　　要：目的 :探讨低氧培养大鼠肺动脉血管内皮细胞VEGF的表达变化与PKC活性的关系。方法 :培养大鼠肺动脉血管内皮细胞 ,观察低氧 (1%O2 )培养不同时间大鼠肺动脉血管内皮细胞浆、膜PKC活性和培养液中VEGF水平变化 ;加入PKC抑制剂 (staurosporine)后 ,测定低氧、常氧培养不同时间二者的变化。结果 :低氧时膜PKC活性和培养液中VEGF水平明显升高 (P <0 .0 1)。而加入PKC抑制剂后 ,常氧和低氧培养的内皮细胞浆、膜PKC活性都明显下降 (P <0 .0 1) ,相应的培养液中VEGF水平与常氧对照组比较无明显变化 (P >0 .0 5 )。结论 :低氧时PKC活性升高与VEGF表达升高有密切关系 ,PKC对低氧时VEGF的表达起正调控作用。Aim:To study the relationship between VEGF expression and PKC activity in pulmonary arterial vascular endothelial cells during hypoxia. Methods:We detected the changes of PKC activity and VEGF levels in pulmonary arterial vascular endothelial cells under the hypoxia,hypoxia with PKC inhibitor and normoxia with PKC inhibitor conditions. Results:It was showed that both PKC activity and VEGF levels increased significantly ( P <0.01) during hypoxia. After adding PKC inhibitor (staurosporine), however,they were both inhibited under the hypoxia and normoxia conditions. Conclusion:Hypoxia stimulates pulmonary arterial vascular endothelial cells to secrete VEGF and PKC may be one of the factors that up-regulate VEGF gene expression during hypoxia.

关 键 词：低氧 肺动脉血管内皮细胞 蛋白激酶 

分 类 号：R331.32[医药卫生—人体生理学]