Smith S F, Tetley T D, Datta A K, Smith T, Guz A, Flower R J
Department of Medicine, Charing Cross and Westminster Medical School, London, United Kingdom.
J Appl Physiol (1985). 1995 Jul;79(1):121-8. doi: 10.1152/jappl.1995.79.1.121.
Lipocortin-1 (LC-1; annexin-1) may mediate some anti-inflammatory actions of the glucocorticoids, probably after binding to specific cell surface binding sites. We have quantified LC-1 levels in bronchoalveolar lavage (BAL) fluid and cells collected from seven healthy volunteers before and after 7 days of treatment with an oral glucocorticoid, prednisolone (30 mg/day). Extracellular BAL LC-1 was higher and cellular LC-1 was lower after prednisolone than before [extracellular: before, median 98 ng/mg albumin (range 48-350 ng/mg albumin); after, 236 ng/mg albumin (19-414 ng/mg albumin); P < 0.05. Cellular: before, 23.3 ng/10(6) cells (14.6-26.9 ng/10(6) cells); after, 18.0 ng/10(6) cells (122-268 ng/10(6) cells); P < 0.05]. The distribution of LC-1 within BAL cells ex vivo (cell surface = 25%, cytosol = 50%, membrane = 25%) was unaffected by prednisolone treatment. However, in adherent cells that had been cultured for 4 h, 70-80% of the LC-1 was on the cell surface. In summary, prednisolone appears to promote cellular release of LC-1. The difference in distribution of cellular LC-1 in BAL cells ex vivo and in vitro may reflect adherence and/or activation.
脂皮质素-1（LC-1；膜联蛋白-1）可能介导糖皮质激素的一些抗炎作用，可能是在与特定细胞表面结合位点结合之后。我们对7名健康志愿者口服糖皮质激素泼尼松龙（30毫克/天）治疗7天前后收集的支气管肺泡灌洗（BAL）液和细胞中的LC-1水平进行了定量。泼尼松龙治疗后，细胞外BAL LC-1水平升高，细胞内LC-1水平降低[细胞外：治疗前，中位数为98纳克/毫克白蛋白（范围为48 - 350纳克/毫克白蛋白）；治疗后，为236纳克/毫克白蛋白（19 - 414纳克/毫克白蛋白）；P < 0.05。细胞内：治疗前，为23.3纳克/10⁶个细胞（14.6 - 26.9纳克/10⁶个细胞）；治疗后，为18.0纳克/10⁶个细胞（12.2 - 26.8纳克/10⁶个细胞）；P < 0.05]。体外BAL细胞内LC-1的分布（细胞表面 = 25%，胞质溶胶 = 50%，细胞膜 = 25%）不受泼尼松龙治疗的影响。然而，在培养4小时的贴壁细胞中，70 - 80%的LC-1位于细胞表面。总之，泼尼松龙似乎促进了LC-1从细胞中释放。体外和体外BAL细胞中细胞内LC-1分布的差异可能反映了细胞贴壁和/或激活情况。
