miR⁃23a⁃5p对脑缺血再灌注氧化损伤的抑制作用研究
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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)


The inhibitory effects of miR⁃23a⁃5p on oxidative damage induced by cerebral ischemia and reperfusion
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    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。

    Abstract:

    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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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(自然科学版),2020,(11):1612-1616

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  • 收稿日期:2019-09-19
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  • 在线发布日期: 2020-12-04
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