中文摘要：

目的探讨糖皮质激素诱导的亮氨酸拉链蛋白（GILZ）在炎症反应过程中的作用机制。方法采用无血清RPMI1640培养基分两组培养人单核细胞株THP-1细胞，其中刺激组加入地塞米松（DEX）刺激，而对照组仅加无血清RPMI1640培养基。12h后提取两组细胞总RNA和总蛋白；用逆转录-聚合酶链反应（RT-PCR）方法在转录水平半定量检测GILZ基因；用蛋白质免疫印迹法（Western blotting）在翻译水平检测核转录因子κB（NF-κB）p65与激活蛋白-1（AP-1）的蛋白表达。收集10例临床创伤患者[创伤严重度评分（ISS）≥16分]伤后24h内的外周血，提取白细胞后分为刺激组和对照组，对照组给予无血清RPMI1640培养基。刺激组在对照组的基础上加入DEX刺激，培养12h后提取白细胞总RNA和总蛋白；用RT-PCR方法在转录水平半定量检测GILZ基因；用Western blotting方法在翻译水平检测NF-κB p65与AP-1的蛋白表达。结果在DEX刺激下，DEX刺激组THP-1细胞和创伤患者外周血白细胞GILZ mRNA表达水平均较对照组升高（P均＜0．01）；DEX刺激组NF-κB p65与AP-1蛋白在THP-1细胞和创伤患者外周血白细胞的表达水平均低于对照组（P均＜0．01）。结论糖皮质激素可上调GILZ基因表达；GILZ的高表达可以抑制NF-κB与AP-1的活性，具有抗炎症反应的作用。

英文摘要：

Objective To investigate the mechanism of the action of glucocorticoid induced leucine zipper （GILZ） in inflammatory reaction. Methods Human monocyte cell line THP - 1 cells were divided into two groups and cultured in nonserum RPMI1640 medium. In one group the cells were treated with dexamethasone （DEX）. Twelve hours later total RNA and total protein were abstracted in both two groups. The mRNA encoding for expression of GILZ was semiquantitatively detected by reserve transcriptasepolymerase chain reaction （RT -PCR）. Protein expression of nuclear factor -κB （NF -κB） p65 and activator protein 1 （AP - 1） were assessed by Western blotting. Peripheral blood of 10 trauma patients Cinjury severity score （ISS） ≥ 16 scores] were collected and the leukocytes were isolated within 24 hours after trauma. The leukocytes were divided into two groups and cultured in nonserum medium. In one group the cells were treated with DEX, Twelve hours later total RNA and total protein were abstracted in both two groups. The mRNA encoding for expression of GILZ was semiquantitatively detected by RT - PCR. Protein expression of NF -κB p65 and AP - 1 were assessed by Western blotting. Results Stimulated by DEX, the expression of GILZ mRNA was increased both in THP - 1 cells and the leukocytes of trauma patients compared with those of control groups （both P〈0.01）, Whereas, protein expressions of NF- κB p65 and AP - 1 of THP - 1 cells and leukocytes in peripheral blood of trauma patients were decreased in the stimulation groups compared with those of control groups （all P〈0.01）. Conclusion The expression of GILZ gene is up-regulated by glucocorticoid. Overexpression of GILZ inhibits NF - κB and AP - 1 activities, suggesting that GILZ possesses anti-inflammatory function.