| 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].现代生物医学进展英文版,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 |
| Received:December 28, 2019 Revised:January 25, 2020 |
| 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） |
| Author Name | Affiliation | | HUO Miao | Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China | | ZHANG Qian | Department of Burn and Plastic Surgery, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China | | ZHANG Yang | Department of Anesthesiology, Huai'an First People's Hospital, Huaian, Jiangsu, 223300, China | | ZHENG Xing-xing | Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China | | CAO Yuan | Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China | | CHEN Xin | Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China |
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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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