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目的研究金钠多对脂多糖(LPS)所致急性肺损伤(ALI)的保护机制及治疗作用。方法采用尾静脉注射脂多糖,按5 mg/kg剂量注射,复制急性肺损伤大鼠模型。将63只Wistar品系大鼠随机分成3组,分别为空白对照组、脂多糖损伤组、金钠多治疗组。各组再随机分为3组,分别为尾静脉注射后2 h、6 h和10 h。利用酶联免疫吸附试验(ELISA)检测血清中可溶性ICAM-1(sICAM-1)水平,肺组织标本分别用免疫组化(定性)和蛋白印迹(定量)方法检测其NFkB核因子。结果尾静脉注射脂多糖可成功复制出急性肺损伤大鼠模型；治疗组血清sICAM-1水平明显高于空白对照组(P＜0．01),损伤组的血清sICAM-1水平明显高于治疗组和空白对照组(P＜0．01)；免疫组化和蛋白印迹实验证实,NF-kB核因子在各组中的阳性表达强度为：金钠多损伤组＞脂多糖治疗组＞空白对照组(P＜0．01)。结论脂多糖可诱导急性肺损伤,金钠多对脂多糖所致的急性肺损伤具有显著的保护作用,其机制可能是抑制了肺组织细胞NF-kB的活性。
Objective To investigate the protective mechanism and therapeutic effects of Jin Na Duo on acute lung injury (ALI) induced by lipopolysaccharide (LPS). Methods The rat model of acute lung injury was duplicated by tail vein injection of lipopolysaccharide and injection at a dose of 5 mg/kg. Sixty-three Wistar strain rats were randomly divided into three groups: blank control group, lipopolysaccharide injury group, and gold sodium treatment group. Each group was randomly divided into 3 groups, 2 h, 6 h and 10 h after tail vein injection. The levels of soluble ICAM-1 (sICAM-1) in serum were detected by enzyme-linked immunosorbent assay (ELISA). The NFkB nuclear factor was detected by immunohistochemical (qualitative) and western blot (quantitative) methods. Results The rat model of acute lung injury was successfully reproduced by tail vein injection of lipopolysaccharide. The serum level of sICAM-1 in the treatment group was significantly higher than that in the control group (P<0.01). The level of serum sICAM-1 in the injury group was significantly higher than that in the treatment group. Group and blank control group (P <0.01); Immunohistochemistry and Western blotting experiments confirmed that the positive expression intensity of NF-kB nuclear factor in each group was: Jin Naduo injury group> lipopolysaccharide treatment group> blank control Group (P < 0.01). Conclusion Lipopolysaccharide can induce acute lung injury. Jin Nao Duo has a significant protective effect on acute lung injury induced by lipopolysaccharide. The mechanism may be that it inhibits the activity of NF-kB in lung tissue.