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在离体肺组织培养模型上观察低浓度 (1～ 10 0pmol/L)内皮素 1(endothelin 1,ET 1)对活性氧所致肺表面活性物质 (pulmonarysurfactant,PS)脂质合成障碍及PS脂质主要组分磷脂酰胆碱合成限速酶CTP :磷酸胆碱二胞苷酰基转移酶 (phosphorylcholinecytidylyltransferase ,CCT)活性的影响。结果显示 :(1)黄嘌呤 黄嘌呤氧化酶超氧阴离子生成系统呈剂量依赖性地降低肺组织 3 H 胆碱的掺入量 ;(2 )ET 1可减轻活性氧所致 3 H 胆碱掺入量的减少和肺组织丙二醛含量的增高 ;但对肺组织超氧化物歧化酶、过氧化氢酶及总抗氧化能力无明显影响 ;(3)ET 1可分别提高和降低肺组织细胞微粒体和胞浆的CCT活性 ,并可减轻活性氧所致肺微粒体CCT活性的降低。结果表明 ,低浓度ET 1具有保护肺微粒体的CCT活性、减轻氧化性肺损伤所致PS合成障碍的作用 ,其保护机制并非通过影响肺组织内源性抗氧化系统而实现
The effects of endothelin 1 (ET 1) at a low concentration (1 ~ 100 pmol / L) on the lipid synthesis of pulmonary surfactant (PS) induced by reactive oxygen species (ROS) Effect of phosphatidylcholine synthesis rate-limiting enzyme CTP: phosphorylcholinecytidylyltransferase (CCT) activity as a major component. The results showed that: (1) xanthine xanthine oxidase superoxide anion generation system in a dose-dependent manner to reduce 3H-choline incorporation in lung tissue; (2) ET 1 can reduce ROS-induced 3H choline incorporation (P <0.05). (3) ET 1 increased and decreased the content of MDA in lung tissue, but did not affect the activities of superoxide dismutase, catalase and total antioxidant capacity in lung tissue. (3) Microsomal and cytoplasmic CCT activity, and can reduce reactive oxygen species lung microsomal CCT activity decreased. The results showed that the low concentration of ET 1 has the function of protecting the CCT activity of lung microsome and alleviating the disorder of PS synthesis induced by oxidative lung injury. The protective mechanism is not achieved by affecting the endogenous antioxidant system of lung tissue