文章摘要
霍 苗,张 倩,张 阳,郑星星,曹 元,陈 欣.七氟醚预处理对大鼠脑缺血再灌注损伤的改善机制[J].,2020,(12):2246-2251
七氟醚预处理对大鼠脑缺血再灌注损伤的改善机制
Mechanism of Sevoflurane Pretreatment on Cerebral Ischemia-reperfusion Injury in Rats
投稿时间:2019-12-28  修订日期:2020-01-25
DOI:10.13241/j.cnki.pmb.2020.12.009
中文关键词: 脑缺血再灌注损伤  七氟醚  TGF-β2 / Smad3信号通路  脑保护  脑梗死
英文关键词: Cerebral ischemia-reperfusion injury  Sevoflurane  TGF-?茁2/Smad3 signaling pathway  Brain protection  Cerebral infarction
基金项目:陕西省自然科学基金项目(2018JQ8023)
作者单位
霍 苗 陕西省人民医院麻醉科 陕西 西安 710068 
张 倩 陕西省人民医院烧伤整形美容医学外科 陕西 西安 710068 
张 阳 江苏省淮安市第一人民医院麻醉科 江苏 淮安 223300 
郑星星 陕西省人民医院麻醉科 陕西 西安 710068 
曹 元 陕西省人民医院麻醉科 陕西 西安 710068 
陈 欣 陕西省人民医院麻醉科 陕西 西安 710068 
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中文摘要:
      摘要 目的:探究七氟醚预处理对大鼠脑缺血再灌注损伤的影响,以及转化生长因子-β2(TGF-β2)/Smad3信号通路的活化情况。方法:将50只SD大鼠随机分为5组(n=10):假手术组、模型组、七氟醚预处理组、吡非尼酮组和七氟醚预处理+吡非尼酮组。通过右颈内动脉(ICA)缝线结扎方法制备脑缺血再灌注(I/R)损伤模型。建模前1h,七氟醚组大鼠吸入2.0%七氟醚1h,吡非尼酮组大鼠腹膜内注射200 mg/kg的TGF-β2抑制剂吡非尼酮,七氟醚+吡非尼酮组大鼠同时应用两种药物处理。再灌注24 h后,通过Zea-Longa五级评分法评价大鼠神经功能缺损评分,处死大鼠并测量梗死体积。通过苏木精-伊红(HE)染色和Nissl染色评价脑组织损伤程度。TdT介导的dUTP缺口末端标记法(TUNEL)分析细胞凋亡。免疫荧光染色和Western blot检测TGF-β2、Smad3、血管内皮生长因子-A(VEGF-A)和CD34的表达情况。结果:七氟醚预处理明显降低了大鼠的脑梗塞面积和神经功能缺损评分。七氟醚预处理抑制了大鼠大脑皮质和海马CA1区的神经元凋亡。七氟醚预处理上调了TGF-β2、VEGF-A和CD34的表达,以及Smad3的磷酸化水平。TGF-β2抑制剂吡非尼酮处理均可减弱七氟醚的脑保护作用并抑制TGF-β2、VEGF-A和CD34的表达和Smad3的磷酸化。结论:七氟醚预处理通过激活TGF-β2/ Smad3信号通路来减轻I/R损伤大鼠的脑损伤。
英文摘要:
      ABSTRACT Objective: To explore the effect of sevoflurane pretreatment on cerebral ischemia-reperfusion injury and the activation of transforming growth factor-β2 (TGF-β2)/Smad3 signaling pathway. Methods: Fifty SD rats were randomly divided into 5 groups (n=10): sham group, model group, sevoflurane pretreatment group, pirfenidone group, and sevoflurane pretreatment + pirfenidone group. A brain I/R model was prepared by suture ligation of the right internal carotid artery (ICA). 1 h before modeling, rats in the sevoflurane group inhaled 2.0% sevoflurane for 1 h, rats in the pirfenidone group were injected intraperitoneally with 200 mg/kg of TGF-β2 inhibitor pirfenidone, rats in the sevoflurane pretreatment + pirfenidone group were treated with two drugs simultaneously. After 24 h of reperfusion, the neurological deficit score of the rats was evaluated by Zea-Longa five-level scale. The degree of brain tissue damage was evaluated by hematoxylin-eosin (HE) staining and Nissl staining. Apoptosis was analyzed by TdT-mediated dUTP nick-end labeling (TUNEL) method. Immunofluorescence staining and Western blot were used to detect the expression of TGF-β2, Smad3, Vascular endothelial growth factor-A (VEGF-A) and CD34. Results: Sevoflurane pretreatment significantly reduced cerebral infarct size and neurological deficit score in rats. Sevoflurane pretreatment inhibited neuronal apoptosis in rat cerebral cortex and hippocampal CA1 region. Sevoflurane pretreatment up-regulated the expression of TGF-β2, VEGF-A and CD34, as well as the phosphorylation level of Smad3. Treatment with the TGF-β2 inhibitor pirfenidone attenuated the brain protective effect of sevoflurane and inhibited the expression of TGF-β2, VEGF-A and CD34 and phosphorylation of Smad3. Conclusion: Sevoflurane pretreatment can reduce brain injury in rats with I/R injury by activating the TGF-β2 / Smad3 signaling pathway.
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