CAJ | 학술논문

目的建立大鼠芥子气(sulfur mustard,SM)肺损伤的动物模型,探讨SM致大鼠ALI的细胞凋亡和氧化应激情况.方法选取雄性大鼠72只,随机分为SM组(32只)、丙二醇对照组(32只)和正常对照组(8只).SM组气管内注入稀释的SM(2 mg/kg,0.1 ml),丙二醇对照组气管内注入丙二醇0.1 ml,正常对照组不做任何处理.通过电镜、免疫组化、BALF观察SM诱导细胞凋亡和氧化应激.结果 SM组:①BALF中乳酸脱氢酶、谷胱甘肽过氧化物酶水平6h达高峰;②Ⅰ型肺泡细胞膜局部缺失,Ⅱ型肺泡细胞表面微绒毛断裂缺失,两者均有线粒体嵴模糊,粗面内质网表面附着的核糖体脱离;③肺泡间隔细胞凋亡明显增多.丙二醇对照组与正常对照组相同.结论细胞凋亡和氧化应激是SM(2 mg/kg)诱导大鼠ALI机制的两大特征.
목적 건립대서개자기(sulfur mustard,SM)폐손상적동물모형,탐토SM치대서ALI적세포조망화양화응격정황.방법 선취웅성대서72지,수궤분위SM조(32지)、병이순대조조(32지)화정상대조조(8지).SM조기관내주입희석적SM(2 mg/kg,0.1 ml),병이순대조조기관내주입병이순0.1 ml,정상대조조불주임하처리.통과전경、면역조화、BALF관찰SM유도세포조망화양화응격.결과 SM조:①BALF중유산탈경매、곡광감태과양화물매수평6h체고봉;②Ⅰ형폐포세포막국부결실,Ⅱ형폐포세포표면미융모단렬결실,량자균유선립체척모호,조면내질망표면부착적핵당체탈리;③폐포간격세포조망명현증다.병이순대조조여정상대조조상동.결론 세포조망화양화응격시SM(2 mg/kg)유도대서ALI궤제적량대특정.
Objective To establish rat model of pulmonary injury induced by sulfur mustard (SM) to investigate the apoptosis and oxidative stress in the injured lung.Methods 72 male rats were selected,then randomly divided into SM group (n =32),propylene glycol group (n =32),and normal control group (n =8).The rats in SM group were injected intratracheally diluted SM (2 mg/kg,0.1 ml),the rats in propylene glycol group were injected intratracheally propylene glycol 0.1 ml,meanwhile the status quo was kept with the normal control group.Then the SM-induced apoptosis and oxidative stress were observed by electron microscope,immunohistochemical staining,and bronchoalveolar lavage fluid (BALF) examination.Results SM group:①The content of lactate dehydrogenase and glutathione peroxidase in BALF peaked in 6h.②There was local defect of cellular membrane in alveolar epithelial type Ⅰ cells,while microvilli missed as well as disarranged in alveolar epithelial type Ⅱ cells.The appearance of ribosome detached from rough endoplasmic reticulum,and illegibility of mitochondrial cristae were observed in both types of cells.③Apoptosis was observed significantly increasing in the alveolar septum.Results in the propylene glycol group was the same with those in the normal control group.Conclusions Apoptosis and oxidative stress are two main mechanism characteristics of SM (2 mg/kg) induced pulmonary injury in rats.