胍丁胺对内毒素诱导的大鼠急性肺损伤的治疗效果

目的：研究胍丁胺对内毒素（ LPS）诱导的急性肺损伤治疗效果及其机制。方法：采用LPS 诱导大鼠急性 肺损伤模型并予以胍丁胺治疗，分为对照组，单纯模型组，低、高剂量胍丁胺治疗组。绘制Kaplan-Meier 生存曲 线观察胍丁胺治疗后大鼠生存率差异，并检测肺组织湿干比及组织炎症情况；检测肺组织中抗氧化酶（SOD）活性、 丙二醛（ MDA）含量；收集肺泡灌洗液并提取肺组织总蛋白，检测肺组织及肺泡灌洗液中炎症因子白细胞介素6 （ IL-6）、肿瘤坏死因子α（ TNF-α）含量。结果：胍丁胺可提高LPS 诱导的大鼠急性肺损伤模型的生存率、显著 降低肺组织的湿重/ 干重比。H-E 染色结果显示胍丁胺可改善肺组织炎症状况。与单纯模型组相比，低、高剂量 胍丁胺治疗组的肺组织MDA 含量下降、SOD活性上调，差异具有统计学意义。ELISA 结果表明，低、高剂量胍 丁胺治疗组的肺组织及肺泡灌洗液中IL-6、TNF-α 分泌降低。结论：胍丁胺可抑制肺部过度氧化应激及炎症反应， 发挥对急性肺损伤的保护作用。

Therapeutic effects of agmatine on lipopolysaccharide-induced acute lung injury in rats

Objective To investigate the therapeutic effects of agmatine on lipopolysaccharide（ LPS）-induced acute lung injury in rats. Methods The acute lung injury in rats was induced by LPS. The rats were divided into control group， simple model（ LPS） group， low-dose agmatine group and high-dose agmatine group. Firstly， the Kaplan- Meier survival curve was drawn to observe the difference in survival rate among these groups. Besides， the wet-todry ratio and pathological changes of lung tissues was detected. Subsequently， the content of superoxide dismutase （ SOD） and malondialdehyde （ MDA） in lung tissues was detected. Finally， alveolar lavage fluid and total protein of lung tissues were collected to measure inflammatory factor content（ IL-6， TNF-α）. Results Agmatine could improve the survival rate of LPS-induced acute lung injury in rats and significantly reduce the wet-to-dry（ W/D） ratio of lung tissues. H-E staining results showed that agmatine could extenuate the inflammation in lung tissues. Moreover， compared with the simple model group， there was a higher level of SOD and a lower level of MDA both in the low and high-dose agmatine treatment group. The results of ELISA showed that the secretion of IL-6 and TNF-α in lung tissues and alveolar lavage fluid of low- and high-dose agmatine treatment group was decreased compared with that of simple model group. Conclusion Agmatine can play a protective role in acute lung injury in rats by inhibiting excessive oxidative stress and inflammatory response.