牛磺酸对大鼠急性肺损伤的保护作用与分子机制

目的：复制脂多糖（lipopolysaccharide,LPS）诱导的大鼠急性肺损伤（acute lung inj ury,ALI）模型,探究牛磺酸（taurine,Tau）对大鼠ALI的保护作用机制。方法：将54只大鼠随机分为3组,每组18只：正常对照组、LPS组和LPS＋Tau 干预组。腹腔注射 LPS（5 mg/kg）建立 ALI 模型,腹腔注射 Tau（5 mg/kg）干预,各组动物分别于注射后3、6、9 h 检测肺组织超氧化物歧化酶（superoxide dismutase,SOD）活性和丙二醛（malonaldehyde,MDA）含量的改变,蛋白印迹法检测 p-p38蛋白在肺组织中的表达变化并在光镜下观察肺组织形态学改变。结果：LPS 组与对照组相应时间点比较,肺组织中的 MDA 含量和 p-p38蛋白表达显著升高（P〈0.01）,而 SOD 活性显著降低（P 〈0.01）；LPS＋Tau 干预组与 LPS 组比较,肺组织MDA含量（P〈0.01）及p-p38蛋白表达明显降低（P 〈0.05,P 〈0.01）,而 SOD 活性明显升高（P〈0.01）,且肺组织的病理改变显著减轻。结论：Tau对大鼠ALI时的肺脏起明显的保护作用,保护机制可能与其抗氧化作用及抑制p38MAPK信号通路的过度激活有关。

Protective Effects and Molecular Mechanism of Taurine in rats of acute Lung Inj ury

Obj ective：To investigate the protective effects and molecular mechanism of taurine （Tau）in lung tissues in rats by repeating lipopolysaccharide（LPS）-induced of acute lung in j ury rat model.Methods：Fifty-four rats were randomly divided into three groups：control group（normal saline was instilled peritoneally）,LPS group （LPS was instilled peritoneally） and PS＋Tau group （LPS was instilled peritoneally followed by Tau）.All rats of each group were sacrificed at different time points （3 h,6 h and 9 h,respectively）after inj ection.Lung tissues were harvested and homogenized to determine change of MDA content and SOD activity.We used Western blot method to detect the expression of p-p38 mitogen-activated protein kinase in lung tissues and used light microscope to observe morphological changes.Results：Compared with control group, MDA content and the expression of p-p38 in lung tissues increased significantly at different time points after injection in LPS group which SOD activity decreased obviously（P 〈0.01）.When compared with LPS group,MDA content in lung tissues decreased obviously（P〈0.01）and the expression of p-p38 decreased in LPS＋Tau group（P 〈0.05,P 〈0.01）,while SOD activity increased significantly（P〈0.01）and inflammatory reaction was lessened significantly.Conclusion：Tau could protect lung tissues of rats from LPS-induced ALI.The protective effect on ALI may attributes to antioxidation and inhibition of over activation of the pathway of p38MAPK.