目的 探讨脂多糖性急性肺损伤大鼠肺组织血管紧张素转换酶的表达变化和可能的作用机制.方法 32只健康雄性Wistar大鼠随机分为正常0.9%氯化钠注射溶液对照组(NS组)、急性肺损伤后6、12、24 h三组(LPS时间组),每组8只,LPS时间组通过股静脉注射LPS(5 mg/kg)建立急性肺损伤模型.NS组给予等量NS.在相应时间点检测血气分析、肺组织湿/干重比(W/D)、HE染色、Real-timePCR方法检测肺组织ACE和ACE2 mRNA表达,免疫组织化学检测ACE和ACE2蛋白表达.结果 LPS组大鼠表现出急性肺损伤症状,随时间点延长,PaO2逐渐降低,肺W/D比值升高(P＜0.05),HE染色显示肺组织损伤明显.LPS组大鼠肺组织ACE mRNA和蛋白表达随时间组延长明显增强(P＜0.05),而ACE2mRNA和蛋白表达却明显减弱(P＜0.05).结论 肺组织ACE、ACE2表达的改变在急性肺损伤大鼠的发病机制中可能起到重要作用.%Objective To observe the expression of angiotensin-converting enzyme (ACE) and ACE2 in rat lung at different time point after acute lung injury induced by LPS and to explore the possible value in mealiating acute lung injury. Methods 32 healthy male Wistar rats were randomly divided into four groups ( n = 8 in each group ) ,ie. a normal control group(NS group) ,and 3 injury groups (LPS group) of 6 h,12 h and 24 h respectively after intravenously injection with LPS (5 mg/kg) to establish the ALI model. The rats were sacrificed at different time point. Arterial blood gas analysis was performed and lung tissue samples were collected for measurement of lung wet/dry weight ratio (W/D) ,HE staining,and ACE and ACE2 expression by immunochemistry and Real-time PCR. Results The injury rats all displayed acute lung injury symptoms. Compared with NS group, PaO2 in LPS group were significantly decreased,whereas the ratio of W/D weight were increased with the time (P ＜ 0. 05 ). The pathologic damage of lung tissue was serious. The expression of ACE in lung tissue was increased immediately after injury while the expression of ACE2 in lung tissue was decreased ( P ＜ 0.05 ). Conclusion The imbalance of expression of ACE and ACE2 in lung might play an important role in the pathogenesis of acute.lung injury.
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