肺间质病病人肺泡巨噬细胞蛋白激酶C活性增高
Increased activity of protein kinase C in alveolar macrophages in idiopathic pulmonary fibrosis
摘要目的 探讨特发性肺纤维化(IPF)患者肺泡巨噬细胞蛋白激酶C(PKC)活性的变化。方法 应用放射活性测定法检测9例健康对照者和15例临床诊断为IPF的患者经纤维支气管镜检查获得的支气管肺泡灌洗液(BALF)中肺泡巨噬细胞的PKC活性。结果 IPF患者BALF肺泡巨噬细胞总PKC活性(57.86±8.60pmol.min-1.mg-1 vs 46.02±11.73pmol.min-1.mg-1)、胞浆(89.83±21.94pmol.min-1.mg-1 vs 65.73±27.91pmol.min-1.mg-1)和胞膜PKC活性(39.67±8.98pmol.min-1.mg-1 vs 32.77±4.96pmol.min-1.mg-1)均明显高于对照组(P<0.01、P<0.05和P<0.05),AM的总PKC活性与BALF中细胞总数呈正相关(r=0.8135,P<0.01), 胞膜PKC活性也与之呈正相关(r=0.5917,P<0.05)。结论 PKC作为细胞活化的信号传导通路与肺间质病的发生发展密切相关。
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abstractsObjective To investigate the changes on protein kinase C (PKC) activity of alveolar macrophages (AMs) in patients with idiopathic pulmonary fibrosis (IPF).Methods The PKC activity of AM in 9 healthy volunteers and 15 patients with IPF was investigated by measuring the radioactivity.Results The total, cytosolic and membrane PKC activity of AM in bronchoalveolar lavage fluid (BALF) from patients with IPF were higher than those from control group (P<0.01, P<0.05 and P<0.05, respectively). The total and the membrane-associated PKC activity had a positive correlation with the number of cells in BALF (r=0.8135, P<0.01 and r=0.5917, P<0.05), respectively. Conclusion As a bypass of transmembrane signal transduction, PKC was suggested to be involved in the origination and development of IPF.
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