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免疫抑制豚鼠肺部炎症反应中TNF-α的表达 被引量:1

Lipopolysaccharide Induced Pulmonary Inflammatory Response and Effects of Tumor Necrosis Factor in Immunocompromised Host
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摘要 目的 探讨免疫抑制宿主 (ICH)肿瘤坏死因子 α(TNF α)介导的肺部炎症机制。方法 采用醋酸可的松联合环磷酰胺建立ICH动物模型 ,ICH活体肺经气管给予内毒素 (LPS)诱导ICH肺部炎症反应 ,刺激前及刺激后 1、3、5、8、2 4h行支气管肺泡灌洗 (BAL) ,异硫氰酸胍一步法抽提肺组织总RNA。随机引物DNA标记方法制备TNF αcDNA探针 ,点杂交测定TNF αmRNA。结果 LPS刺激后肺组织病理发现有急性炎症反应 ,支气管肺泡灌洗液 (BALF)中细胞数随LPS刺激时间延长而增加 ,于 5h达高峰 ,肺泡巨噬细胞 (PAM)和中性粒细胞(PMN)数量均增高 ,但PAM比例因PMN比例升高而降低。TNF α在LPS刺激后 5h达高峰 ,2 4h降至接近刺激后 1h的水平。BALF中TNF浓度明显高于血清的浓度。BALF中TNF水平的增高与PMN进入肺泡腔在动力学上基本平行。肺脏组织TNF αmRNA于LPS刺激后逐渐上升 ,于 3h达高峰 (4 5 .47± 2 .0 4) ,之后缓慢下降 ,其表达超前于TNF分泌峰值。结论 TNF可能是介导PMN内流和炎症的细胞因子 (CKs)之一。ICH过高的TNF释放会引起肺损伤。在受到LPS刺激后ICH系统性炎症免疫反应抑制而肺部炎症依然剧烈 ,反映了“腔室化” Purpose To investigate the pulmonary inflammatory response and TNF mediated effects in immunocompromised host(ICH). Materials and Methods Pulmonary Inflammation in ICH Model & Specimen Obtain:hartley strains healthy male guinea pigs were divided into 8 groups.There are ten animals in each group.ICH model of guinea pigs were induced by receiving daily intraperitoneal injections of cyclophophamide(15 mg·kg -1 ·d -1 )plus daily subcutaneous injections of cortisone acetate(100 mg·kg -1 ·d -1 )for a total of 7 consecutive days.We challenged guinea pigs intratracheally with LPS 200 μg/animal,experimental animals were anaesthetized before and 1,3,5,8,24 hours after challenged,respectively(five animals in each group).Move out lung,quickly freeze in liquid nitrogen,stored at -70?℃ .Another experimental animals were lavaged before and 1,3,5,8,24 hours after lipopolysaccharide(LPS)challenge,respectively(five animals in each group).Total RNA was extracted from lung tissue by single step method of guanidine thiocyanatephenol chloroform and then stored at -70?℃.Dilute the RNA sample in RNA dilution buffer(30 μg),spot the RNA sample onto a dry positively charged nylon membrane. RNA Dot blotting and immuological detection were performed to detect tumou necrosis factor α(TNF α)mRNA,which were partly improved.The density of hybridization signal was analyzed via image system. Results Five hours after LPS challenged,total counts of bronchoalveolar fluid(BALF)cells and the propotion of PMN increased significently.Although the counts of both PAM and PMN increased,the propotion of PAM decreased gruadually accompanied by increase of the propotion of PMNs.Hematoxylin eosin stained lung sections after challenged with LPS show and acute intraalveolar inflammatory response.After intratracheal injection of LPS,the TNF level in BALF progressively increased.Both the TNF level and PMF counts started to increased at 1 hour after LPS challenge,peaked at 5 hours.The TNF level in serum did not increase mark
出处 《上海医科大学学报》 CSCD 2000年第5期346-349,共4页 Journal of Fudan University(Medical Science)
关键词 肿瘤坏死因子-Α 免疫抑制宿主 肺部炎症反应 tumor necrosis factor-α immunocompromised host inflammatory
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参考文献3

  • 1兰锡纯主编..心脏血管外科学[M].北京:人民卫生出版社,1984:474.
  • 2Zhong W W,Arch Surg,1993年,128卷,158页 被引量:1
  • 3Ulich T R,Am J Pathol,1990年,137卷,1173页 被引量:1

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