摘要
目的探讨内皮一氧化氮合成酶(Endothelial nitric oxide synthase,eNOS)与热休克蛋白90(Heat shock protein90,HSP90)在肺动脉高压(PH)发病机制中的关系与作用。方法以持续性肺动脉高压的胎羊模型(PH组)为研究对象,以正常胎羊为对照(NC组),利用免疫沉淀和Western印迹等技术,检测各组胎羊肺动脉内皮细胞eNOS和HSP90的表达量及eNOS和HSP90两者的结合情况。结果PH组内皮eNOS的表达水平、eNOS和HSP90结合量与NC组相比均呈显著性降低(P<0.05)。结论PH形成时内皮和eNOS功能受损,表现为eNOS的表达或eNOS与HSP90结合量的减少,导致NO生成减少而氧自由基增加。
Objective To understand the relationship between endothelial nitric oxide synthase (eNOS) and Heat shock protein (HSP90) in pathogenesis of pulmonary hypertension. Methods 8 fetal lambs were divided into two groups, pulmonary hypertension group (PH) and normal control group (NC). The level of eNOS and HSP90 and the interaction of eNOS with HSP90 were determined by immunopreeipitation and western blot. Results The level of eNOS and the combination of eNOS to HSP90 in PH group were lower than those in NC group ( P 〈 0.05). Conclusion Decreased HSP90 - eNOS interactions may contribute to the impaired NO and enhanced oxygen free radical in fetal lambs with persistent pulmonary hypertension.
出处
《中国热带医学》
CAS
2006年第8期1365-1367,共3页
China Tropical Medicine
基金
广东省卫生厅科研基金资助项目(A2005302)
关键词
肺动脉高压
内皮一氧化氮合酶
热休克蛋白90
Pulmonary hypertension
Endothelial nitric oxide synthase
Heat shock protein