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目的：观察雷米普利时急性肺损伤(ALI)时肺组织核因子-κB(NF-κB)活性的影响。方法：SD大鼠随机分为正常对照组(NS组)、内毒素损伤组(LPS组)和雷米普利预防组(RAM组),用免疫组织化学法检测肺组织NF-κB的表达,并进行肺系数测定以及肺组织炎症细胞计数；光镜下观察大鼠肺组织的病理形态学变化。结果：LPS组肺组织NF-κB表达比NS组增强(P＜0．05),肺系数和炎症细胞数比NS组增加(P＜0．05),肺组织损伤改变严重；RAM组NF-κB表达比LPS组降低(P＜0．05),肺系数和炎症细胞数较LPS组减少(P＜0．05),肺组织损伤程度也减轻。结论：NF-κB活化在LPS诱导的AL1中起重要作用,雷米普利可降低NF-κB的活性,减轻LPS导致的ALI。
Objective: To observe the effect of ramipril on acute lung injury (ALI) in lung tissue when nuclear factor-κB (NF-κB) activity. Methods: SD rats were randomly divided into normal control group (NS group), endotoxin injury group (LPS group) and Ramipril prevention group (RAM group). The expression of NF-κB in lung tissue was detected by immunohistochemistry, The pulmonary coefficient was measured and the number of inflammatory cells in lung tissue was counted. The pathological changes of lung tissue were observed under light microscope. Results: The expression of NF-κB in lung tissue of LPS group was higher than that of NS group (P <0.05), and the number of pulmonary and inflammatory cells increased compared with that of NS group (P <0.05) κB expression was lower than that of LPS group (P <0.05), the number of pulmonary and inflammatory cells decreased compared with LPS group (P <0.05), and the degree of lung injury also decreased. Conclusion: Activation of NF-κB plays an important role in LPS-induced AL1. Ramipril can reduce the activity of NF-κB and decrease the ALI induced by LPS.