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目的利用改良的基因表达综合分析(SAGE)技术监测内毒素诱发小鼠急性肺损伤的基因表达状况,探讨急性肺损伤的分子机制。方法气管内注射内毒素(25mg/kg)复制急性肺损伤模型。正常对照小鼠气管内注射等体积等渗盐水。内毒素注射24h后以氯胺酮深度麻醉后处死小鼠,整块取出肺脏用于SAGE研究。建立正常和急性肺损伤两个SAGE标记物文库。结果正常文库包括24670个SAGE标记物,代表12168个基因。急性肺损伤文库包括26378个SAGE标记物,代表13397个基因。急性肺损伤组有11种基因升高10倍以上,107种基因升高5-10倍,2121种基因升高2-5倍。7种基因表达降低大于10倍,87种基因降低5-10倍,1571种基因降低2-5倍。结论证实了内毒素诱导的急性肺损伤发生机制中各种基因表达的变化,并发现了以往没有报道的基因。对这些基因功能的进一步研究有助于阐明急性肺损伤的发生机制,并为临床诊断提供有参考价值的血清标记物。
OBJECTIVE: To monitor the gene expression of acute lung injury induced by endotoxin in mice by a modified gene expression analysis (SAGE) technique and to explore the molecular mechanism of acute lung injury. Methods Endotoxin (25mg / kg) was injected intratracheally to replicate acute lung injury model. Normal control mice were intratracheally injected with an equal volume of isotonic saline. Twenty-four hours after the injection of endotoxin, the mice were sacrificed after deep anesthesia with ketamine, and the whole lung was removed for SAGE study. Establish two SAGE marker libraries for normal and acute lung injury. Results The normal library consisted of 24670 SAGE markers, representing 12,168 genes. The acute lung injury library includes 26,378 SAGE markers, representing 13,397 genes. In the group of acute lung injury, 11 genes increased more than 10 times, 107 genes increased 5-10 times and 2121 genes increased 2-5 times. Seven genes were reduced more than 10-fold, 87 genes by 5-10-fold, and 1571 genes by 2-5-fold. Conclusions The endotoxin-induced changes in the expression of various genes in the pathogenesis of acute lung injury were confirmed, and no previously reported genes were found. Further studies on the function of these genes help elucidate the pathogenesis of acute lung injury and provide valuable serum markers for clinical diagnosis.