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目的探讨乌司他丁对脂多糖(LPS)致小鼠急性肺损伤的作用及其机制。方法小鼠腹腔注射乌司他丁(50和100 ku.kg-1)或等体积生理盐水30 m in后,分别静脉注射LPS 15 mg.kg-1或等体积生理盐水,于注射LPS后不同时间检测有关各项指标。ELISA法测定血清和肺组织中TNFα水平,RT-PCR法测定TNFαmRNA和iNOS mRNA的表达。W estern b lotting法检测c-Fos,c-Jun及iNOS等蛋白表达。结果乌司他丁100 ku.kg-1能显著降低LPS引起的小鼠的肺脏指数、肺组织及血清中NO水平的增加,下调肺组织c-Jun蛋白表达量和iNOS mRNA及其蛋白的表达量,而对小鼠的血清和肺组织冲洗液中TNFα含量以及肺组织MDA无明显影响。结论乌司他丁对LPS引起的小鼠肺损伤有保护作用,该作用与其抑制c-Jun蛋白和iNOS mRNA的表达有关。
Objective To investigate the effect of ulinastatin on lipopolysaccharide (LPS) -induced acute lung injury in mice and its mechanism. Methods After intraperitoneal injection of ulinastatin (50 and 100 ku · kg-1) or an equal volume of normal saline for 30 min, mice were injected with LPS 15 mg · kg-1 or an equal volume of normal saline, respectively, after injection of LPS Time to detect the various indicators. The levels of TNFα in serum and lung tissue were measured by ELISA and the expression of TNFαmRNA and iNOS mRNA were detected by RT-PCR. W estern b lotting assay c-Fos, c-Jun and iNOS and other protein expression. Results Ulinastatin 100 ku.kg-1 could significantly reduce the LPS-induced lung index, lung tissue and serum NO levels, down-regulated c-Jun protein expression and iNOS mRNA and protein expression However, there was no significant effect on the level of TNFα in the serum and lung tissue of mice and MDA in lung tissue. Conclusion Ulinastatin has a protective effect on LPS-induced lung injury in mice, which is related to the inhibition of c-Jun protein and iNOS mRNA expression.