摘要
目的 观察脂多糖 (LPS)介导的急性肺损伤 (ALI)大鼠肺组织白介素 13(IL 13)mRNA表达的变化 ,探讨ALI发生、发展过程中抗炎机制变化的意义。 方法 (1)由鼠尾静脉注射梯度剂量LPS ,制作ALI模型 (APDS)。 (2 )逆转录PCR法检测肺组织IL 13mRNA含量。 结果 (1)梯度剂量LPS可以引发不同程度的ALI,当LPS≥ 6mg/kg时 ,大鼠出现急性呼吸窘迫综合征 (ARDS)。 (2 )LPS可以导致肺组织IL 13mRNA表达升高 ,当LPS≥ 6mg/kg时 ,IL 13mRNA表达增加显著。 结论 (1)尾静脉注射LPS可以复制大鼠ALI模型。 (2 )LPS≥ 6mg/kg是大鼠发生ARDS的临界剂量。 (3)LPS诱导大鼠肺组织IL 13mRNA表达增强 。
Objective To observe the change in IL 13 mRNA expression in rat lungs with acute lung injury (ALI) induced by lipopolysaccharide (LPS), so as to investigate the significance of anti inflammatory mechanism in the development of ALI. Methods (1) Different doses (2~8 mg/kg) of LPS were injected via the tail vein to the rats to establish ALI model. (2) The IL 13 mRNA content in pulmonary tissue was determined by RT PCR. Results (1) Different degrees of ALI was induced in the rats by different doses of LPS. ARDS was produced in the rats by LPS of 6mg/kg. (2) The IL 13 mRNA expression in the pulmonary tissue could be enhanced by the induction of LPS, especially when its dose was larger than 6 mg/kg. Conclusion (1) Rat ALI model could be produced by LPS injection via the tail vein. (2) LPS in dose of 6 mg/kg was the threshold for the production of rat ARDS. (3) The incidence of rat ARDS might be closely related to the enhanced expression of IL 13 mRNA in rat pulmonary tissue.
出处
《中华烧伤杂志》
CAS
CSCD
2002年第3期145-148,共4页
Chinese Journal of Burns
基金
国家自然科学基金重点资助项目 (3 973 0 2 10 )
军队医学科学技术研究"十五"重点资助项目 (0 12 0 74)