摘要
目的 探讨内皮素 (ET) - 1m RNA和原癌基因 bcl- 2在大鼠内毒素性休克肺损伤中的作用及山莨菪碱、地塞米松对肺的保护作用。 方法 2 4只 SD大鼠随机分为 4组 (n=6 ) : 组 (对照组 )静注等量生理盐水 ; 组 (休克组 )静脉注射脂多糖 (L PS) 5 m g/kg; 组静注山莨菪碱 4m g/kg后 0 .5 h再静注 L PS 5 m g/kg; 组静注地塞米松 4mg/kg后 0 .5 h再静注 L PS 5 mg/kg。观察 5 h后取肺组织测定 ET- 1m RNA和 bcl- 2。 结果 肺组织 ET- 1m RNA表达 , 、 组与 组比较差异无显著性 , 组与 、 、 组比较差异有非常显著性 (P<0 .0 1)。bcl- 2阳性细胞率 组轻微增加 , 、 组显著增加 , 组阴性表达。 结论 ET- 1m RNA和 bcl- 2可介导大鼠内毒素性休克时肺的损伤。山莨菪碱和地塞米松可能是通过抑制 ET- 1m RNA的表达和促进 bcl- 2的表达而起到对肺的保护作用。
Objective\ To study the role of ET\|1 mRNA and bcl\|2 and the protective effect of anisodamine and dexamethasone in lung injury induced by endotoxic shock.\ Methods\ Twenty\|four SD mice were randomly divided into four groups(each group n=6).\ In group Ⅰ and Ⅱ,saline or lipopolysacharide(LPS) 5 mg/kg was administrated intravenously.\ In group Ⅲ and Ⅳ,anisodamine or dexamethasone was administrated at half an hour before LPS administration.\ The expression of ET\|1 mRNA and bcl\|2 of the lung tissue after five hours were analyzed by RT\|PCR and immunohistochemical method.\ Results\ Expression of ET\|1 mRNA in lung tissue of group Ⅱ was enhanced significantly compared with groupⅠ,Ⅲ,Ⅳ(P<0 01).\ There is no significant difference in group Ⅲ,Ⅳ compared with group Ⅰ.\ Percent rate of cells with bcl\|2 expression increased markedly in group Ⅲ,Ⅳ,and only slightly in group Ⅱ.\ There was no expression in groupⅠ.\ Conclusion\ ET\|1 mRNA and bcl\|2 may induce lung injury in endotoxic shock.\ Anisodamine and dexamethasone could protect lung injury induced by endotoxic shock,and its mechanism might involve ET\|1 mRNA inhibition and bcl\|2 enhancement.\;
出处
《福建医科大学学报》
2000年第3期218-220,共3页
Journal of Fujian Medical University
关键词
内毒素性休克
肺损伤
内皮素-1
mRNA
山莨菪碱
genes expression
apoptosis
shock
endotoxic
lung injury
anisodamine
dexamethasone
rat
