论文部分内容阅读
目的 :观察白介素 1β(IL 1β)在内毒素 (LPS)所致急性肺损伤 (ALI)发病过程中的作用及神农 33(SN33)注射液对ALI大鼠的保护作用。 方法 :Wistar大鼠尾静脉注射LPS ,建立ALI模型。分别采用ELISA和NorthernBlotting方法检测不同时相血清中IL 1β含量及肺组织IL 1βmRNA水平的变化 ;同时以地塞米松为对照 ,观察SN33对IL 1β基因表达的影响。光镜、电镜观察大鼠肺病理形态学变化。 结果 :LPS诱发大鼠ALI过程中血清IL 1β水平显著高于正常对照组 (P <0 .0 1) ,峰值为LPS攻击后 2h ;肺组织IL 1βmRNA表达明显增高 ,峰值为LPS攻击后 1h ;以SN33保护的大鼠 ,IL 1β含量和mRNA表达均明显低于相应时相LPS攻击组 ;且肺损伤程度减轻。 结论 :IL 1β在LPS诱导的ALI过程中起着重要作用 ;SN33注射液可以抑制IL 1β的释放和表达 ,对肺脏有一定的保护作用。
OBJECTIVE: To investigate the role of interleukin-1β (IL-1β) in the pathogenesis of acute lung injury (ALI) induced by endotoxin (LPS) and the protective effect of SN33 injection on ALI rats. Methods: LPS was injected into tail vein of Wistar rats to establish ALI model. The levels of IL-1β and IL-1βmRNA in lung tissue were detected by ELISA and Northern blotting respectively. The effect of SN33 on the expression of IL-1β was also observed by dexamethasone. Light and electron microscope observation of pathological changes of lung in rats. Results: The level of IL-1β in LPS-induced ALI was significantly higher than that in normal control group (P <0.01), the peak value was 2h after LPS challenge. The expression of IL-1βmRNA in lung tissue was significantly increased, with the peak value being 1 h after LPS challenge. The level of IL-1β and the mRNA expression of SN33-protected rats were significantly lower than those of the corresponding LPS-treated groups, and the extent of lung injury was relieved. CONCLUSION: IL 1β plays an important role in LPS-induced ALI. SN33 injection can inhibit the release and expression of IL 1β and has some protective effects on the lung.