内毒素致伤大鼠肺组织促炎与抗炎细胞因子mRNA表达的时相性研究  

Studies on the expression of mRNA of anti - and pro -inflammatory cytokines in acute lung injury induced by lipopolysaccharide in rat

作　　者：张青[1] 李琦[1] 毛宝龄[1] 钱桂生[1] 徐剑铖[1] 陈正堂[1] 

机构地区：[1]第三军医大学新桥医院呼吸病研究所,重庆400037

出　　处：《中国危重病急救医学》2004年第10期585-588,共4页Chinese Critical Care Medicine

基　　金：国家自然科学基金重点资助项目(39730210)

摘　　要：目的 研究不同剂量内毒素致伤大鼠肺组织促炎和抗炎细胞因子mRNA表达的时相性,并探讨这些细胞因子在全身炎症反应失控和急性肺损伤中的可能作用。方法 采用逆转录-聚合酶链反应(RT-PCR)检测不同剂量脂多糖(LPS)致伤大鼠肺组织肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β、IL-6、IL-4、IL-10和IL-13的mRNA表达。结果 随着LPS剂量增加,TNF-α、IL-1β、IL-6、IL-4、IL-10和IL-13的mRNA表达均增强(与生理盐水对照组比较,P均<0.01);LPS≥6 mg/kg组上述细胞因子表达显著高于此剂量以下组(P均<0.01)。表达峰值时间:TNF-α为1 h,IL-6为4 h,其他均在2 h。结论 内毒素致急性肺损伤中,TNF-α是早期表达的促炎细胞因子,而IL-6在炎症进一步发展中发挥作用;抗炎细胞因子IL-4、IL-10、IL-13高表达亦可能促进炎症的放大而不是起保护作用。Objective To study the role of pro - inflammatory cytokines including tumor necrosis factor - α (TNF - α) , interleukin -1β(IL - 1β) , IL - 6 , and anti - inflammatory cytokines including IL - 4, IL - 10, and IL - 13 in acute lung injury(ALI). Methods Reverse transcription - polymerase chain reaction (RT-PCR) were used to assess the expressions of mRNA of TNF-α, IL - 1β, IL-6, IL-4, IL - 10 and IL - 13 in the lung tissue after lipopolysaccharide challenge. Results The expression of TNF -α mRNA was seen to peak at 1 hour and IL-6 mRNA at 4 hours in lung tissue after the challenge. The highest expression of mRNA of other cytokines, such as IL - 1β, IL-4, IL - 10 and IL - 13 in lung tissue appeared 2 hours after LPS - induced lung injury. Conclusion TNF - a is an early presenting cytokine in ALI, and IL-6 may play an important role in delayed development of ALI. The over - expression of anti - inflammatory cytokines IL-4, IL - 10 and IL - 13 may act as promoters rather than protectors in amplification of inflammatory process.

关 键 词：肿瘤坏死因子 白细胞介素 抗炎症因子 促炎症因子 全身炎症反应综合征 肺损伤 急性 

分 类 号：R363[医药卫生—病理学]