| 顾晓燕,杜 强,潘化平,冯 慧,付 娟,梅程瑶,纪 纤,张保国.脑缺血大鼠肺组织NGF/TrkA表达变化及其意义[J].现代生物医学进展英文版,2020,(2):255-258. |
| 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 |
| Received:June 23, 2019 Revised:July 18, 2019 |
| DOI：10.13241/j.cnki.pmb.2020.02.010 |
| 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:南京市江宁区科技发展计划项目（2018C056）；江苏省第十二批六大人才高峰项目（WSN015） |
| Author Name | Affiliation | E-mail | | GU Xiao-yan | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | guxiaoyan05@163.com | | DU Qiang | Department of Respiratory Medicine, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210011, China | | | PAN Hua-ping | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | | | FENG Hui | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | | | FU Juan | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | | | MEI Cheng-yao | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | | | JI Xian | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | | | ZHANG Bao-guo | Department of Rehabilitation, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, Jiangsu, 211100, China | |
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| 中文摘要: |
| 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6 h、24 h及48 h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6 h肺组织W/D有增加，差异无统计学意义（P>0.05），而脑缺血后24 h及48 h肺组织W/D均有显著增高(P < 0.05 )，其中以24 h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，24 h及48 h组肺泡结构破坏明显。病理学评分结果显示，脑缺血后24 h及48 h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6 h肺组织中NGF表达增加(P <0.05)，48 h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)，24 h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: |
| ABSTRACT Objective: To investigate the dynamic expressions of nerve growth factor (NGF). And its tyrosinekinase A (TrkA ) receptor in lung tissue of rats with cerebral ischemia. Methods: Thirty two adult male SD rats were randomly divided into four groups using a random number table ( n = 8each): Sham-operated group, Cerebral ischemia group (6 h, 24 h, 48 h). We established a rat model of cerebral ischemia by permanent middle cerebral artery occlusion (pMCAO). At different time points after pMCAO, the rats were sacrificed and lung tisues were excised for analysis of wet/dry (W/D) weight ratio and HE examination. A t the same time, the expression of NGF 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 24 h 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 in 24 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 24 h 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 6 h after cerebral ischemia (P > 0.05), decreased significantly at 24 h (P < 0.05), and increased at 48 h, 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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