CAJ | 학술논문

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。
목적：복제지다당(lipopolysaccharide,LPS)유도적대서급성폐손상(acute lung inj ury,ALI)모형,탐구우광산(taurine,Tau)대대서ALI적보호작용궤제。방법：장54지대서수궤분위3조,매조18지：정상대조조、LPS조화LPS+Tau 간예조。복강주사 LPS(5 mg/kg)건립 ALI 모형,복강주사 Tau(5 mg/kg)간예,각조동물분별우주사후3、6、9 h 검측폐조직초양화물기화매(superoxide dismutase,SOD)활성화병이철(malonaldehyde,MDA)함량적개변,단백인적법검측 p-p38단백재폐조직중적표체변화병재광경하관찰폐조직형태학개변。결과：LPS 조여대조조상응시간점비교,폐조직중적 MDA 함량화 p-p38단백표체현저승고(P<0.01),이 SOD 활성현저강저(P <0.01)；LPS+Tau 간예조여 LPS 조비교,폐조직MDA함량(P<0.01)급p-p38단백표체명현강저(P <0.05,P <0.01),이 SOD 활성명현승고(P<0.01),차폐조직적병리개변현저감경。결론：Tau대대서ALI시적폐장기명현적보호작용,보호궤제가능여기항양화작용급억제p38MAPK신호통로적과도격활유관。
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 LPS+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.