论文部分内容阅读
目的 :探讨当归与硝苯吡啶对慢性支气管炎 (慢支 )肺泡巨噬细胞胞浆游离钙水平的影响。方法 :对慢支缓解期患者 7例和正常对照者 6例进行支气管肺泡灌洗获得的肺泡巨噬细胞经分离、纯化后 ,加Fura- 2 /AM负载 ,以Fura - 2荧光比值法测定加当归、硝苯吡啶及LPS后胞浆游离钙的水平。结果 :慢支组肺泡巨噬细胞胞浆中基础钙水平 (189 47± 2 3 6 9)nmol/L较正常对照组 (99 6 5± 32 2 1)nmol/L明显增高 (P <0 0 1) ;LPS促进慢支组肺泡巨噬细胞包括胞内钙库释放引起的胞浆游离钙水平升高 (基础钙 189 47± 2 3 6 9nmol/L ;LPS组 2 35 5 3± 30 30nmol/L) (静息钙 2 2 8 41± 2 7 36nmol/L ;氯化钙 +LPS组 2 88 47± 43 6 8nmol/L) (P均 <0 0 1) ;当归及硝苯吡啶均抑制LPS对慢支组肺泡巨噬细胞胞浆游离钙水平的升高作用 (静息钙 2 2 8 41± 2 7 36nmol/L ;氯化钙 +当归 +LPS组 2 36 6 8± 2 8 6 0nmol/L ;氯化钙 +硝苯吡啶 +LPS组 2 5 2 6 4± 37 0 5nmol/L) (P均>0 0 5 )。结论 :当归与硝苯吡啶通过抑制慢支患者肺泡巨噬细胞胞浆游离钙水平升高 ,影响肺泡巨噬细胞的活化 ,对于慢支气道内的非特异性炎症可能具有抑制作用
Objective: To investigate the effect of Angelica sinensis and nifedipine on cytoplasmic free calcium in alveolar macrophages of chronic bronchitis (chronic bronchitis). Methods: The alveolar macrophages obtained from bronchoalveolar lavage of 7 patients with chronic bronchitis and 6 normal controls were isolated, purified, and loaded with Fura - 2 / AM. Fura - 2 fluorescence ratio assay Angelica, nifedipine and LPS after cytoplasmic free calcium levels. Results: The basal calcium level in cytoplasm of alveolar macrophages in chronic bronchitis group (189 47 ± 23 36 9 nmol / L) was significantly higher than that in normal control group (99 6 ± 32 2 1 nmol / L) (P 0 00 1). LPS promoted the increase of cytoplasmic free calcium levels in alveolar macrophages of chronic bronchitis group including intracellular calcium release (basal calcium 189 47 ± 23 6 9 nmol / L; LPS group 2 35 53 ± 30 30 nmol / (P <0.01); Angelica sinensis and nifedipine all inhibited LPS (resting calcium 2 2841 ± 2 7 36nmol / L; calcium chloride + LPS group 2 88 47 ± 43 6 8nmol / L) (Ca2 + 2 +8 41 ± 2 7 36nmol / L), calcium chloride + Angelica + LPS group (2 368 ± 2860nmol / L; calcium chloride + nifedipine + LPS group 2 5 2 6 4 ± 37 0 5nmol / L) (P> 0 05). Conclusion: Angelica sinensis and nifedipine may inhibit the nonspecific inflammation in chronic bronchitis by inhibiting the increase of cytosolic free calcium levels in alveolar macrophages, inhibiting the activation of alveolar macrophages