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作 者:刘富春[1] 黄一[1] 李学成[1] 罗艳梅[1] 高军[1] 张浩[1]
机构地区:[1]中国人民解放军第三二四医院药剂科,重庆404100
出 处:《重庆医学》2015年第23期3187-3189,3194,共4页Chongqing medicine
基 金:重庆市卫生局医学科研项目(2013-2-302)
摘 要:目的探讨前列腺素E1(PGE1)对肺撞击伤后肺泡细胞凋亡的影响。方法雄性SD大鼠分为正常对照组、伤后对照组和伤后PGE1处理组。致伤后24h检测动脉氧分压、肺系数,TUNEL染色检测肺泡细胞凋亡的整体情况。以蛋白免疫印迹试验(Western blot)检测自噬相关蛋白及自噬调节蛋白NIX的表达情况。结果伤后24h肺组织可见明显结构破坏及肺水肿。与正常对照组相比,伤后对照组动脉氧分压降低(P<0.05),肺泡细胞凋亡指数增加(P<0.05),同时肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白NIX表达增加(P<0.05)。伤后PGE1处理组动脉氧分压低于正常对照组(P<0.05),但较伤后对照组显著改善(P<0.05);肺泡细胞凋亡指数高于正常对照组,但显著低于伤后对照组(P<0.05);肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白NIX的表达虽然较正常对照组增加(P<0.05),但显著低于伤后对照组(P<0.05)。结论PGE1减轻大鼠肺撞击伤后肺泡细胞凋亡,此作用可能是通过抑制NIX介导的细胞自噬,以及肺泡细胞自噬性凋亡实现。Objective To investigate the effect of prostaglandin E1(PGE1)on alveolar cells apoptosis in rat lung impact injury model.Methods SD rats were divided into 3groups(normal control group,lung injury control group and PGE1 treated group).PaO2 and pulmonary coefficient were detected after 24 hof impact.TUNEL labeling was used to evaluate apoptosis and Western blot was used to estimate protein expression levels of beclin-1,LC3Ⅱ/LC3Ⅰand NIX.Results After 24 hof impacting,there were obvious structural damage and pneumonedema in rat lung.Compared to normal control group,the PaO2 of lung injury control group decreased and the apoptosis of alveolar cells increased significantly(P〈0.05).Furthermore,the expression levels of Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the impacting control group were increased(P〈0.05).In the PGE1 treated group,the PaO2 were decreased compared to normal control group(P〈0.05),but these expression levels were higher significantly than lung injury control group(P〈0.05).The expression levels of apoptosis,Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the PGE1 treated group were increased compared to normal control group(P〈0.05),but these expression levels were lower significantly than lung injury control group(P〈0.05).Conclusion PGE1 could alleviate alveolar cells apoptosis after lung impacting injury,and which effect may ascribe to PGE1 inhibiting NIX-mediated autophagy and autophagic apoptosis of alveolar cells.
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