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作 者:徐睿[1] 祝筱姬[3] 孟晓[1] 赵超[3] 连承进[3] 王涛[4] 季鹏[3] 鞠玲燕[4] 王美红[4] 张圣明[2]
机构地区:[1]潍坊医学院研究生部,261042 [2]潍坊医学院电镜室,261042 [3]解放军第89医院呼吸科,潍坊261021 [4]解放军第89医院病理科,潍坊261021
出 处:《国际呼吸杂志》2014年第14期1063-1068,共6页International Journal of Respiration
摘 要: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(2mg/kg,0.1ml),丙二醇对照组气管内注人丙二醇0.1ml,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(2mg/kg)诱导大鼠ALI机制的两大特征。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 ratsin propylene glycol group were injected intratracheally propylene glycoI 0. 1 ml,meanwhile the status quo was kept with the normal control group. Then the SM-induced apoptosis and oxidative stress wereobserved by electron microscope,immunohistochemical staining, and bronchoalveolar lavage fluid (BALF) examination. Results SM group: ①The content of lactate dehydrogenase and glutathione peroxidase inBALF 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 ofribosome 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.
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