摘要
目的 :探讨山莨菪碱对脓毒症大鼠肺组织生物喋呤产生的影响及其意义。方法 :采用大鼠盲肠结扎穿孔 (CL P)致脓毒症模型 ,动物随机分为正常对照组、脓毒症组和山莨菪碱治疗组。分别于 CL P后 2、8、16小时处死动物 ,检测肺组织生物喋呤及其合成限速酶三磷酸鸟苷环水解酶 I(GTP CHI) m RNA表达和肿瘤坏死因子α(TNFα) m RNA表达的改变。结果 :脓毒症动物肺组织生物喋呤含量显著升高 ,GTP CHI基因表达水平也显著增强 ,而且其改变与局部 TNFα m RNA表达水平呈正相关。给予山莨菪碱治疗后 2小时 ,组织生物喋呤含量、GTP CHI m RNA表达及 TNFα m RNA表达水平均明显下降 (P<0 .0 5或 P<0 .0 1) ,且肺组织髓过氧化物酶活性也显著降低 (P<0 .0 5 )。结论 :脓毒症早期应用山莨菪碱能有效抑制肺组织生物喋呤及其合成限速酶基因表达 。
Objective:To evaluate the potential effect of anisodamine on pulmonary biopterin induction in a rat model of sepsis.Methods:Wistar rats were subjected to sepsis induced by cecal ligation and puncture(CLP),and animals were randomly divided into normal controls(n=6),sepsis group (n=18),as well as anisodaminetreated group (n=18).Animals were sacrificed at 2,8,16 hours after CLP.Biopterin levels,guanosine triphosphate cyclohydrolase I(GTPCHI) mRNA expression,and tumor necrosis factorα(TNFα) mRNA expression of pulmonary tissue were measurd in animals at various intervals.Also,pulmoary tissue myeolperoxidase(MPO) activities were determined at 2 hours after CLP.Results:After CLP,pulmonary tissue biopterin and GTPCHI mRNA expression levels were markedly increased (all P<0 01),and the latter was significantly correlated with local TNFα mRNA expression (P<0 05).Treatment with anisodamine,however,tissue biopterin levels,GTPCHI gene expression and TNFα gene expression levels were markedly reduced together with decrease in pulmonary MPO activities (P<0 05).Conclusions:Early treatment with anisodamine has an inhibitory effect on pulmonary GTPCHI mRNA expression and biopterin synthesis as well as its release,and it may protect against acute lung injury in rats following CLPinduced sepsis.
出处
《中国危重病急救医学》
CAS
CSCD
2000年第10期591-594,共4页
Chinese Critical Care Medicine
基金
国家重点基础发展规划项目!(No.G19990542032)
国家自然科学基金资助项目!(No.39870286)
军队杰出中青年人才专项基金资助项目!(No.9
关键词
脓毒症
盲肠结扎穿孔术
生物喋呤
山莨菪碱
sepsis
cecal ligation and puncture
biopterin
anisodamine
acute lung injury
