| 二苯乙烯苷抑制NADPH氧化酶对小鼠脑缺血/再灌注损伤的保护作用 |
| |
| 引用本文： | 薛威,唐虹,孙雨倩,江勤,黄大可,董六一.二苯乙烯苷抑制NADPH氧化酶对小鼠脑缺血/再灌注损伤的保护作用[J].中国实验动物学报,2019(2):208-214. |
| |
| 作者姓名： | 薛威 唐虹 孙雨倩 江勤 黄大可 董六一 |
| |
| 作者单位： | 安徽医科大学药理学教研室;安徽医科大学临床医学院;安徽医科大学基础医学院 |
| |
| 基金项目： | 安徽省自然科学基金(1408085MH174)~~ |
| |
| 摘 要： | 目的探讨二苯乙烯苷(TSG)抑制NADPH氧化酶对小鼠脑缺血再灌注(I/R)损伤的保护作用。方法将100只实验小鼠随机分成5组:假手术组、模型组,TSG低剂量组(3 mg/kg),TSG中剂量组(6 mg/kg),TSG高剂量组(12 mg/kg),每组20只。通过双侧颈总动脉结扎造成小鼠脑缺血2 h,再灌注24 h后处死小鼠。采用HE染色法对小鼠脑组织进行病理学检测,采用DHE染色法和ESR波谱仪检测脑组织中活性氧(ROS)水平,采用Western blot法检测脑组织中NOX4和cleaved caspase-3/9蛋白的表达。结果小鼠脑缺血再灌注后,缺血区皮层脑组织出现严重的病理性损伤,其ROS水平显著升高,脑组织中NOX4蛋白表达显著上调,凋亡相关蛋白cleaved caspase-3/9蛋白表达量显著增加。TSG可以显著减轻小鼠缺血再灌注脑组织的病理性损伤,抑制ROS的产生,显著下调氧化应激蛋白NOX4的表达,并显著抑制凋亡相关蛋白cleaved caspase-3/9蛋白的表达。结论 TSG可通过抑制脑组织氧化应激蛋白NOX4的表达,减少活性氧的生成,并抑制凋亡相关蛋白cleaved caspase-3/9过度表达,对小鼠脑缺血再灌注损伤起保护作用。
|
| 关 键 词： | 二苯乙烯苷 脑缺血再灌注 NADPH氧化酶 活性氧 凋亡 小鼠 |
Tetrahydroxystilbene glucoside protects against cerebral ischemia/reperfusion injury by inhibiting expression of NADPH oxidase in mice |
| |
| XUE Wei,TANG Hong,SUN Yuqian,JIANG Qin,HUANG Dake,DONG Liuyi.Tetrahydroxystilbene glucoside protects against cerebral ischemia/reperfusion injury by inhibiting expression of NADPH oxidase in mice[J].Acta Laboratorium Animalis Scientia Sinica,2019(2):208-214. |
| |
| Authors: | XUE Wei TANG Hong SUN Yuqian JIANG Qin HUANG Dake DONG Liuyi |
| |
| Affiliation: | (Key Laboratory of Chinese Medicine Research and Development, State Administration of TCM, Anhui Medical University;Clinic Medical College of Anhui Medical University;Basic Medical School of Anhui Medical University, Hefei 230032, China) |
| |
| Abstract: | XUE Wei;TANG Hong;SUN Yuqian;JIANG Qin;HUANG Dake;DONG Liuyi(Key Laboratory of Chinese Medicine Research and Development, State Administration of TCM, Anhui Medical University;Clinic Medical College of Anhui Medical University;Basic Medical School of Anhui Medical University, Hefei 230032, China) |
| |
| Keywords: | SG cerebral ischemia reperfusion NADPH oxidase ROS apoptosis mice Conflicts of Interest: The authors declare no conflict of interest |
| 本文献已被 维普 等数据库收录！ |
|
