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作 者:李文军[1] 宗城[2] 吉天鹏[1] 杨晓东[1] 张宏[1] 张斌[1] 李二红[1] 赵广贺[1]
机构地区:[1]解放军第159医院全军烧伤中心,河南驻马店463000 [2]第三军医大学西南医院烧伤研究所,重庆400038
出 处:《细胞与分子免疫学杂志》2002年第1期13-15,共3页Chinese Journal of Cellular and Molecular Immunology
摘 要:目的 探讨内毒素(LPS)和地塞米松(Dex)对体外培养的大鼠肺泡巨噬细胞(AM)中NF-KB活化的影响,以及AM中NF-KB活化在急性肺损伤中的可能作用。方法 通过建立大鼠AM体外培养技术,应用免疫组化染色法,观察LPS和Dex寸 AM中 NK-KBP~(65),IKB-α、TNF-α和 ICAM-l蛋白表达的动态变化。结果 LPS能使培养的AM中 NF-KBP~(65),TNF-α和ICAM-l的表达增加,IKB-α的表达降低;Dex的作用与 LPS恰相反。结论LPS促进AM中的NF-KB活化,可能是急性肺损伤肺内炎症损害发生的启动及促进因素;Dex抑制 NF-KB的活化,可能是其抗炎作用的重要机制之一。Aim To explore the effects of LPS and Dex on NF- KB activation of cultured alveolar macrophages ( AMs) and to study the role of AMs in the pathogenesis of acute lung injury. Methods AMs were harvested by bronchoalveolar lavage technique ,and cul- tured in vitros. The influences of LPS and Dex on expression of NF- KB^(65) ,IKB- α、TNF- α and ICAM- 1 proteins in the AMs were evalu- ated at the different time points ( 2,6, 12 and 24 hours after cul- ture) by immunohistochemical staining. Results LPS could in- crease the expression of NF- KB P^(65),TNF- α、and ICAM- 1 proteins and decrease 1KB- α in the AMs. The influences of Dex on the ex- pression of these proteins were contrary to those of LPS. Conclu sion LPS can promote NF- KB activation in AMs , which may contribute to the pathogenesis of acute lung injury. Dex can inhibit NF- KB activation in AMs ,which may be a mechanism of anti - in- flammation by Dex.
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