蛋白激酶Cδ亚型抑制剂对脂多糖诱导肺微血管内皮细胞损伤的影响  

Effect of PKCδ inhibitor on permeability injury of pulmonary microvascular endothelial cells monolayer induced by lipopolysaccharide

作　　者：朱钟鸣[1] 孙耕耘[1] 

机构地区：[1]安徽医科大学第一附属医院呼吸内科,安徽合肥230022

出　　处：《中国药理学通报》2006年第7期800-803,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No3007334);安徽省卫生厅第一层次学术和技术带头人培养计划资助项目

摘　　要：目的研究蛋白激酶C(PKC)的亚型PKCδ在大鼠肺微血管内皮细胞(RPMVEC)中的表达及其抑制剂Rottlerin对脂多糖(LPS)导致RPMVEC单层通透性增高的影响。方法取体外培养的RPMVEC进行PKCδ的W estern b lot和免疫组化检测,用针头式滤器检测LPS及LPS+Rottlerin干预后RPMVEC单层滤过系数(K f)的变化。结果PKCδ在RPMVEC中有广泛的表达,其表达部位主要位于胞质。Rot-tlerin能减低LPS导致的RPMVEC单层通透性增高。结论LPS导致RPMVEC损伤的机制与PKC的激活有关,PKCδ亚型抑制剂可减轻LPS诱导的RPMVEC单层通透性增高。Aim To study the expression of protein kinase C （PKC） subtype PKCδ in rat pulmonary microvascular endothelial cell （ RPMVEC ） , and the effect of its inhibitor （Rottlerin） on LPS-induced RPMVEC monolayer permeability injury. Methods In cultured RPMVEC, Western blot and immunohistochemistry were used to identify the expression of PKCδ. Microinfiltrator was used to measure the changes of RPMVEC monolayer permeability coefficient （Kf） after exposure to LPS or LPS with Rotterin together. Result We found a high level of PKCδ expression in cytoplasm. Rottlerin could obviously inhibit the increase of LPS-induced RPMVEC Kf value. Conclusion The activation of PKC is involved in the progress of LPS-induced RPMVEC injury. Furthermore, the inhibitor of PKCδ could release LPS-induced RPMVEC Kf increase.

关 键 词：蛋白激酶C 脂多糖类 内皮细胞 通透性 

分 类 号：R-322[医药卫生] R322.13