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作 者:王万铁[1] 陈瑞杰[2] 郝卯林[1] 倪世容[1] 王青[1] 王方岩[1] 宋张娟[1] 金可可[1] 王卫[1] 郑绿珍[1] 汪洋[1]
机构地区:[1]温州医学院病理生理学教研室,浙江温州325035 [2]温州医学院附属第二医院药剂科,浙江温州325027
出 处:《中国急救医学》2006年第10期674-677,共4页Chinese Journal of Critical Care Medicine
基 金:浙江省教育厅科研基金(No.20000670);温州市科技计划重点项目(No.Y2005A080)
摘 要:目的探讨左旋精氨酸对肺缺血/再灌注损伤(PIRI)时Fas/FasL表达的影响。方法采用在体兔单肺原位缺血/再灌注模型。实验兔30只,随机分为假手术对照组(C组)、肺缺血/再灌注组(I/R组)和肺缺血/再灌注加左旋精氨酸组(L-Arg组),每组10只。分别于再灌注3h取左肺组织,观察Fas/Fas配体(Fas/FasL)mRNA定位表达、凋亡指数(AI)、肺组织湿干质量比(W/D)、肺损伤组织学定量评价指标(IQA)及光镜、电镜下的组织形态学改变。结果L-Arg组Fas/FasL mRNA在肺小动脉内(外)膜、肺小静脉内膜、肺泡上皮及肺支气管上皮呈弱阳性表达,明显低于L/R组(P<0.05);AI、W/D和IQA值显著低于L/R组(P<0.01和P<0.05);肺组织形态学异常改变不同程度减轻。结论左旋精氨酸可下调肺组织Fas/FasL mRNA的表达而减轻细胞凋亡,对PIRI发挥积极的防治作用。Objective To investigate the effect of L - arginine ( L - Arg) on expression of Fas/FasL mRNA during pulmonary ischemia and reperfusion injury (PIRI) in the rabbits. Methods Single lung ischemia and reperfusion animal model was used in vivo. The rabbits were randomly into three groups ,control group (C, n = lO) ,ischemia/reperfusion group (I/R, n = lO) and I/R + L - arginine group ( L - Arg, n = lO). Changes of several parameters which included apoptotic index (AI) , wet to dry ratio of lung tissue weight(W/D) and index of quantitative assessment of histologic lung injury (IQA) were measured at 180 minutes after reperfusion in lung tissue. Meanwhile the location and expression of Fas / FasL mRNA were observed, lung tissue was prepared for light microscopic and electron microscopic observation at 60,180,300 minutes after reperfusion. Results As compared with group I/R, Fas/FasL mRNA slightly expressed in intima and extima of small pulmonary artery, alveoli, and bronchiole epithelia in L - Arg group. The values of AI, W/D and IQA showed significantly lower than that in I/R group at 180 minutes after reperfusion in lung tissue ( P 〈 0.01 and P 〈0.05 ). Meanwhile, abnormal changes of the lung tissue in morphologically were lessen markedly in L - Arg group. Conclusion L - arginine produces notable protective effects on PIRI in rabbits by inhibiting Fas/FasL mRNA express in lung tissue, decreasing apoptosis.
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