脂多糖对离体大鼠胸主动脉和肺组织HO-1mRNA及蛋白表达的影响

Effects of lipopolysaccharide on hemeoxygenase-1 mRNA and hemeoxygenase-1 protein expression in isolated rat thoracic aorta and pulmonary tissue

目的 观察离体大鼠胸主动脉和肺组织脂多糖（Lipopoysaccharide,LPS）孵育后血红素氧合酶-1（HO-1）mRNA及蛋白表达时间依从性的变化。方法24只Wistar大鼠颈椎脱臼处死,取其胸主动脉和肺组织,随机分成四组:对照组（n=6）,实验组包括LPS3、8、24组（均为n=6）,分别与LPS（1μg/ml）孵育3、8、24h。采用蛋白免疫杂交（Western blot）和半定量聚合酶链反应（RT-PCR）分别测定HO-1蛋白和mRNA表达。结果 与对照组相比,胸主动脉HO-1蛋白表达LPS3组即达最高值（P<0.05）,LPS8和LPS24组仍处于较高水平（P<0.05）;肺组织HO-1蛋白表达LPS3组已开始升高（P<0.05）,LPS8组达最高水平（P<0.01）,LPS24组有下降趋势,但仍与对照组有差异（P<0.05）。与对照组相比,胸主动脉HO-1mRNA表达LPS3组即达最高值（P<0.05）,LPS8组较LPS3组无明显变化（P>0.05）,而LPS24组则恢复至初始水平;肺组织HO-1mRNA表达LPS3组开始升高（P<0.05）,LPS8组达到最大值（P<0.01）,LPS24组回到基础水平（P>0.05）。结论 脂多糖可以明显促进大鼠胸主动脉和肺组织HO-1mRNA及蛋白表达,且两种组织表现出不同的时间依从性变化,可能与感染性休克体肺循环不同变化的病生理机制有关。

ve To evaluate the effects of lipopolysaccharide (LPS) on hemeoxygenase-1 (HO-1) mRNA and HO-1 protein expression in isolated rat thoracic aorta (TA) and pulmonary tissue (PT), trying to explain the mechanism of different patho-physiological changes of systemic and pulmonary circulation in septic shock. Methods Twenty-four Wistar rats of either sex weighing 250-400g were sacrificed by cervical spine dislocation. Thoracic aorta and lung tissue were removed under aseptic condition. They were randomly divided into four groups of six animals each: control group (C) and three test groups in which TA and PT were incubated with LPS (1μg·ml-1) for 3h (group LPS3), 8h(group LPS8) and 24h (group LPS24) respectively. HO-1 mRNA expression and HO-1 protein expression in TA and PT were detected by RT-PCR and Western Blot. Results (1) As compared with that in group C, HO-1 protein expression in TA reached peak level in group LPS3, and the peak level was maintained in groups LPS8 and LPS24; while in PT HO-1 protein expression started increasing in group LPS3 and peaked in group LPS8 and tended to decline in group LPS24 but the difference in HO-1 protein expression between group C and LPS 24 was still significant. (2) As compared with that in control group, the HO-1 mRNA expression in TA peaked in LPS3, the peak level was maintained in LPS 8, but it returned to baseline level in LPS 24; while in PT HO-1 mRNA expression started increasing in LPS 3 and peaked in LPS 8 and returned to baseline level in LPS 24. Conclusions LPS can significantly enhance HO-1 mRNA and protein expression in isolated rat thoracic aorta and pulmonary tissue but the time-course is somewhat different between the two tissues. This may explain the different patho-physiologic changes of systemic and pulmonary circulation in septic shock.