文章摘要
脑缺血大鼠肺组织NGF/TrkA表达变化及其意义
Dynamic expressions of nerve growth factor and its tyrosinekinase A receptor in lung tissue of rats with lung injury induced by cerebral ischemia
投稿时间:2019-06-04  修订日期:2019-06-04
DOI:
中文关键词: NGF  TrkA  脑缺血  肺损伤
英文关键词: NGF  TrkA  cerebral ischemia  acute lung injury
基金项目:
作者单位邮编
顾晓燕* 南京市江宁医院 211100
潘化平 南京市江宁医院 
冯慧 南京市江宁医院 
付娟娟 南京市江宁医院 
梅程瑶 南京市江宁医院 
纪纤 南京市江宁医院 
张保国 南京市江宁医院 
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中文摘要:
      目的 探讨大鼠脑缺血后肺组织神经生长因子(nerve growth factor,NGF)/酪氨酸蛋白激酶A(tropomyosin-related kinase A,TrkA)表达的变化。方法成年雄性大鼠随机分为假手术组和脑缺血后6h、24h及48h组,每组8只。建立大脑中动脉永久性局灶性缺血模型,术后于各时间点麻醉处死大鼠后,测定肺组织湿重/干重(W/D),光镜下观察HE染色肺组织病理学改变;Western blot法检测肺组织NGF、TrkA蛋白表达。结果与假手术组相比,脑缺血后6h肺组织W/D有增加,差异无统计学意义(P>0.05),而脑缺血后24h及48h肺组织W/D均有显著增高(P < 0.05 ),其中以24h组最明显(P< 0.01);脑缺血后6 h肺组织出现轻度充血、水肿及炎性改变,24h及48h组肺泡结构破坏明显。病理学评分结果显示,脑缺血后24h及48h组大鼠肺组织病理评分较假手术组显著升高(P<0.05);Western blot法显示,脑缺血6h肺组织中NGF表达增加(P <0.05),48h时表达有下降趋势,但仍高于假手术组(P<0.05)。而肺组织中TrkA表达在脑缺血6h有下降(P >0.05),24h下降明显(P <0.05),48 h时TrkA蛋白表达虽有上升,仍显著低于假手术组(P < 0.05)。结论大鼠肺组织NGF/TrkA的动态变化可能参与了脑缺血后肺损伤的病理生理过程。
英文摘要:
      Objective:To investigate the dynamic expressions of nerve growth factor (NGF) Anditstyrosinekinase A (TrkA ) receptor in lung tissue of ratswithcerebral ischemia.Methods: Thirtytwo adult male SD ratswere randomly divided intofourgroups using a random number table ( n = 8each):Sham-operated group,Cerebral ischemia group (6h,24h,48h).Cerebral ischemia modelwereestablished by permanent middle cerebral artery occlusion(pMCAO). Then the rats weresacrificed at different time points, lung tisues were excised for analysis of wet/dry (W/D) weight ratio and HE examination. A t the same time,the expressionofNGF and TrkA in lung tissues were detected by Western Blot analysis.Results:Compared with sham-operated group, W/D of lung tissue increased significantly at 24h and 48h after cerebral ischemia (P < 0.05), especially in 24h group (P < 0.01).Mild hyperemia, edema and inflammatory changes were observed in lung tissue at 6 hours after cerebral ischemia. While the destruction of alveolar structure was obvious at 24 and 48 hours after cerebral ischemia. The pathological score of lung tissues in24 and 48 hours was significantly higher than that in sham-operated group(P<0.05).Interestingly, the expression of NGF in lung tissue increased at 24h after cerebral ischemia (P < 0.05), but decreased at 48h, which still higher than that in sham-operated group (P < 0.05); TrkA began to decrease at 6h after cerebral ischemia (P > 0.05), decreased significantly at 24h (P < 0.05), and increased at 48h, but still significantly lower than that in sham-operated group (P <0.05).Conclusion:The dynamic changes of NGF/TrkA in rat lung tissue may be involved in the pathophysiological process of lung injury after cerebral ischemia.
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