匹那地尔对慢性阻塞性肺疾病患者肺泡巨噬细胞胞质游离钙浓度及其分泌的NO IL-6的影响

目的观察匹那地尔对慢性阻塞性肺疾病(COPD)患者肺泡巨噬细胞(AM)胞质游离钙浓度及其分泌的一氧化氮(NO)、白细胞介素-6(IL-6)的影响。方法采用支气管肺泡灌洗、细胞培养和荧光指示剂方法,测定AM内钙浓度及其生成的NO和IL-6含量。结果①慢性支气管炎患者肺泡巨噬细胞内钙浓度、NO和IL-6均较对照组胞内钙浓度、NO和IL-6增高(P<0.01);②脂多糖(LPS)刺激以后,胞内游离钙浓度、NO和IL-6均较刺激前增高(P<0.01);③先加匹那地尔孵育AM再加入LPS,胞质内游离钙浓度、NO和IL-6较仅加LPS时减少(P<0.01)。结论匹那地尔可抑制LPS引起的Ca2+]i增加,对LPS刺激的NO和IL-6升高也有抑制作用;匹那地尔可调节AM激活,抑制NO和IL-6分泌。

Effects of Pinacidil on cytosolic free calcium in alveolar macrophages and on macrophage-derived NO and IL-6 in patients with chronic obstructive pulmonary disease

Objective To examine the effects of Pinaeidil on cytosolic free calcium in alveolar macrophages and on macrophages-derived NO and IL-6. Methods Techniques of bronchoalveolar lavage, cell culture-and fluorescent calcium labeling with Fura-2/AM were employed to assess the eeytosolic levels of calcium and secretionof NO an IL-6. Results （（1）Ca2＋]i, NO and IL-6 were significantly increased in chronic bronchitis, as compared with the control group （P〈0.01）. （2）Ca2＋]i, NO and IL-6 were filrther elevated after stimulation with LPS （P〈0.01）. （3）Addifion of LPS after Pinacidil incubation was shown to result in lowered level of Ca2＋]i and less secretion of NO and IL-6（P〈0.01）compared with addition of LPS alone. Conclusion Pinacidil may inhibit the LPS-stimulated increase in Ca2＋]i and secretion of NO and IL-6. It was also shown to downregulate alveolar macrophages activation and suppress the elevation of the NO and IL-6.