摘要
目的探讨还原型谷胱甘肽（GsH）对脓毒症大鼠急性肺损伤保护作用的机制。方法采用盲肠结扎穿孔术（CLP）复制SD大鼠脓毒症模型。按随机数字表法将大鼠分为假手术组、模型组、GSH组、左氧氟沙星（LEV）组；分别于术后3、6、12、24h各取7只大鼠心脏血检测血浆肿瘤坏死因子-α（TNF—α）、白细胞介素-6（IL～6）水平，电镜下观察术后24h大鼠肺组织超微结构的改变。结果与假手术组（（132士9）bLg／L]比较，模型组术后6h血浆TNF—α水平[（227±28）μg／L]显著升高P〈0．01）；GSH治疗组[（144±28）μg／L3较模型组显著降低，且明显低于LEV组[（214±48）μg／L，均P〈0．013；各组问术后3、12、24hTNF—α水平比较均无明显差异。与假手术组[（135．43±40．08）μg／L]比较，模型组术后3h血浆IL-6水平（（267．65±72．87）μg／L]显著升高（P〈0．01）；GSH治疗组[（191．97±62．98）μg／L]较模型组显著降低，且明显低于LEV组[（268．75±74．67）gg／L，均P〈0．053；各组间术后6、12、24hIL～6水平均无明显差异。模型组大鼠肺组织超微结构发生显著变化，尤其是细胞内线粒体出现水肿甚至空泡变性；GSH组大鼠肺组织超微结构的改峦解微。结论TNF—α和IL-6在脓毒疖大鼠肺榀伤发毕机制中韶雷兽作用．GSH有明昂的治疗靳栗．
Objective To investigate the protection mechanism of reduced glutathione （GSH） in acute lung injury in rats with sepsis. Methods Sepsis in Sprague-Dawley （SD） rats were reproduced by cecal ligation and puncture （CLP）. They were randomly divided into four groups, sham-operated group, model group, GSH treatment group and levofloxacin （LEV） treatment group. Heart blood of 7 rats in all groups was collected at 3, 6, 12, 24 hours after operation. The plasma levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） were measured. The lung ultrastructure changes were observed with electron microscope at 24 hours in all groups. Results Compared with the sham-operated group, the plasma level of TNF-α increased more obviously at 6 hours of the model group [（227!28） μg/L vs. （1324-9） μg/L, P〈 0.01]. Compared with the model group, the plasma level of TNF-a in the GSH treatment group decreased obviously [（144 i 28） μg/L3, and it was obviously lower than that of LEV treatment group [（214 i 48） μg/L, both P〈0. 013. No obvious difference of plasma level of TNF-α was found at 3, 12, 24 hours among all the groups. Compared with the sham-operated group, the plasma level of IL-6 of the model group raised obviously at 3 hours [（267. 65±72.87） μg/L vs. （135.43±40. 08） μg/L, P〈0. 013. In the GSH treatmeht group, the plasma level of IL-6 [（191.97± 62.98） μg/L] was lower than that of the model group and the LEV treatment group [（268.75±74.67） μg/L, both P〈0. 05）. The plasma level of IL-6 was not obviously different among all groups at 6, 12, 24 hours. In the model group, the injury of pulmonary ultra- structure was obvious, especially in the mitochondria of the pulmonary cells. In the GSH treatment group, the change in ultrastrueture of the lung was slight. Conclusion TNF-α and IL-6 play significant role in the development of pulmonary ultrastructure injury in acute lung injury of septic rats. Treatment with GSH was effective in preventing such injury.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2010年第5期282-284,I0001,共4页
Chinese Critical Care Medicine
