文章摘要
黄 荣,马 娟,牛 博,李 晋,常 剑,张岩睿,刘 鹏,栾新平.miR⁃23a⁃5p对脑缺血再灌注氧化损伤的抑制作用研究[J].南京医科大学学报,2020,(11):1612~1616
miR⁃23a⁃5p对脑缺血再灌注氧化损伤的抑制作用研究
The inhibitory effects of miR⁃23a⁃5p on oxidative damage induced by cerebral ischemia and reperfusion
投稿时间:2019-09-19  
DOI:10.7655/NYDXBNS20201107
中文关键词: 微小RNA  脑缺血再灌注  氧化损伤
英文关键词: microRNA  cerebral ischemia reperfusion  oxidative stress
基金项目:新疆维吾尔自治区创新环境(人才、基地)建设专项(自然科学基金)联合基金(2018D01C302)
作者单位
黄 荣 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054新疆医科大学第二附属医院神经外科新疆 乌鲁木齐 830028 
马 娟 新疆医科大学第一附属医院神经外科新疆 乌鲁木齐 830011 
牛 博 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054 
李 晋 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054 
常 剑 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054 
张岩睿 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054 
刘 鹏 新疆医科大学第五附属医院神经外科新疆 乌鲁木齐 830054 
栾新平 新疆医科大学第二附属医院神经外科新疆 乌鲁木齐 830028 
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中文摘要:
      目的:探讨miR?23a?5p对大鼠脑缺血再灌注氧化应激反应的抑制作用。方法:应用qPCR技术检测大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)SD大鼠模型中miR?23a?5p的表达水平。使用miR?23a?5p过表达慢病毒注射MCAO大鼠,设置假手术组、对照病毒组和miR?23a?5p病毒组。Berdron评分与2,3,5?三苯基氯化四氮唑(2,3,5?triphenyltetrazoliumchloride,TTC)染色检测大鼠的神经损伤和脑梗死体积。化学比色法测定总超氧化物歧化酶(superoxide dismutase,SOD)与锰超氧化物歧化酶(manganese superoxide dismutase,MnSOD)含量,ELISA检测3?硝基酪氨酸(3?nitrotyrosine,3?NT)与一氧化氮(nitric oxide,NO)含量。采用H2O2处理大鼠中枢神经细胞B35细胞,构建氧化损伤模型。使用miR?23a模拟物转染细胞,设置对照组、miR?23a组、H2O2组和H2O2 +miR?23a组。化学比色法检测总SOD与MnSOD含量,ELISA检测3?NT与NO含量。结果:MCAO大鼠缺血再灌注后,miR?23a?5p的表达迅速降低,随后逐渐升高。miR?23a?5p过表达后可降低Berdron评分与脑梗死体积,降低大鼠血清中3?NT与NO含量,提高总SOD和MnSOD含量。B35细胞中miR?23a?5p过表达降低3?NT与NO胞内水平,上调总SOD和MnSOD水平。结论:miR?23a?5p可以抑制脑缺血再灌注氧化损伤。
英文摘要:
      Objective:This study aims to investigate the inhibitory effect of miR?23a?5p on oxidative stress in rats with cerebral ischemia?reperfusion. Methods:The expression of miR?23a?5p in middle cerebral artery occlusion(MCAO) rat model was detected by qPCR assay. MCAO rats were injected with miR?23a?5p lentivirus and 3 groups were seted: Sham group,NC virus group and miR?23a?5p virus group. The nerve damage were evaluated by Berdron score and cerebral infarction volume were evaluated by 2,3,5?triphenyltetrazoliumchloride(TTC)staining. The total superoxide dismutase(SOD)and manganese superoxide dismutase(MnSOD)contents were determined by chemical colorimetry. The contents of 3?nitrotyrosine(3?NT)and nitric oxide(NO)were detected by ELISA. B35 cells,the central nerve cells of rats,were treated with H2O2 to establish oxidative damage mode and 4 groups were seted:control group,miR?23a group,H2O2 group and H2O2+miR?23a group. The total SOD and MnSOD contents were detected by chemical colorimetry,and the contents of 3?NT and NO were detected by ELISA. Results:After ischemia?reperfusion in MCAO rats,the expression of miR?23a?5p decreased rapidly and then gradually increased. In vivo,the overexpression of miR?23a?5p reduced the Berdron score and cerebral infarction volume,decreased the 3?NT and NO levels in serum,increased the total SOD and MnSOD levels. In B35 cells,the overexpression of miR?23a?5p decreased the intracellular levels of 3?NT and NO whereas increased the levels of total SOD and MnSOD. Conclusion:miR?23a?5p can inhibit oxidative damage induced by cerebral ischemia and reperfusion.
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