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中国临床药理学与治疗学 ›› 2018, Vol. 23 ›› Issue (11): 1215-1220.doi: 10.12092/j.issn.1009-2501.2018.11.003

• 基础研究 • 上一篇    下一篇

miR-145通过调节SOD活性介导人参皂苷Rb1对脑缺血再灌注损伤大鼠的脑保护作用

徐慧1, 张民远2, 戴勤学2   

  1. 1衢州市人民医院麻醉科,衢州 324000,浙江;2温州医科大学附属第一医院麻醉科,温州 325000,浙江
  • 收稿日期:2018-08-13 修回日期:2018-09-09 出版日期:2018-11-26 发布日期:2018-11-22
  • 通讯作者: 戴勤学,男,博士,主治医师,研究方向:脏器保护。 Tel: 13695842272 E-mail: 653091408@qq.com
  • 作者简介:徐慧,女,本科,主任医师,研究方向:脏器保护。 Tel: 1315700768 E-mail: 1308293638@qq.com
  • 基金资助:

    国家自然科学基金资助项目(81704180)

MiR-145 regulating SOD activity mediated brain protection of ginsenosides Rb1 in rats with cerebral ischemia-reperfusion injury

XU Hui1,ZHANG Minyuan2, DAI Qinxue2   

  1. 1 Department of Anesthesiology, Quzhou People's Hospital, Quzhou 324000, Zhejiang, China; 2 Department  of  Anesthesiology, the  First  Affiliated  Hospital  of  Wenzhou  Medical University, Wenzhou 325000, Zhejiang, China
  • Received:2018-08-13 Revised:2018-09-09 Online:2018-11-26 Published:2018-11-22

摘要:

目的: 探讨人参皂苷Rb1是否通过减少miR-145含量来上调脑缺血再灌注损伤大鼠脑组织SOD活性发挥脑保护作用。方法: 将60只SD大鼠按随机数字表法分成模型组、生理盐水对照组、人参皂苷Rb1组、人参皂苷Rb1+miR-145模拟物组、人参皂苷Rb1+miR-145质控品组,每组12只。采用大脑中动脉闭塞(MCAO)法建立大鼠脑缺血再灌注损伤模型。人参皂苷Rb1组和生理盐水对照组大鼠在制模后即刻分别腹腔注射人参皂苷Rb1(40 mg/kg)和等量生理盐水;人参皂苷Rb1+miR-145模拟物组和人参皂苷Rb1+miR-145质控品组大鼠在制模前2 d分别侧脑室注射miRNA 145模拟物和miRNA 145质控品,其他操作同人参皂苷Rb1组。再灌注损伤后24 h测各组大鼠神经行为学评分,其中6只大鼠测量脑梗死体积;另6只大鼠取大脑皮质,测定miR-145、超氧化物歧化酶(SOD)含量。结果: 与模型组比较,人参皂苷Rb1组大鼠行为学评分明显降低(P<0.05),脑梗死体积明显减小(P<0.05),miR-145含量明显减少(P<0.05),SOD活性明显增加(P<0.05)。与人参皂苷Rb1组,人参皂苷Rb1+miR-145模拟物组大鼠行为学评分明显升高(P<0.05),脑梗死体积明显增加(P<0.05),miR-145含量明显增加(P<0.05),SOD活性显著下降(P<0.05)。结论: 人参皂苷Rb1可以通过减少miR-145含量来上调脑缺血再灌注损伤大鼠脑组织SOD活性发挥脑保护作用。

关键词: 脑缺血再灌注损伤, 人参皂苷Rb1, miR-145, 超氧化物歧化酶

Abstract:

AIM: To explore whether ginsenosides Rb1 can increase the activity of SOD in the brain tissue of rats with cerebral ischemia reperfusion injury by reducing the miR-145 content, and play the role of brain protection. METHODS: Sixty SD rats were randomly divided into five groups: model group, normal saline control group, ginsenosides Rb1 group, ginsenosides Rb1+miRNA-145 mimics group and ginsenosides Rb1+miRNA-145 mimics NC group, 12 rats in each group. The rats' cerebral ischemia reperfusion injury models were established by thread embolism method to form middle cerebral artery occlusion (MCAO). After modeling, the rats in ginsenosides Rb1 and saline control group were given ginsenosides Rb1 and normal saline respectively. Two days before modeling, the rats in ginsenosides Rb1+miRNA-145mimics and ginsenosides Rb1+miRNA-145 mimics NC group received miRNA-145 mimics and miRNA-145 mimics NC through lateral ventricle, and other operations were same to ginsenosides Rb1 group. Twenty-four hours after cerebral ischemia reperfusion injury, the cerebral tissues were taken and the volume of cerebral infarction was measured in 6 rats in each group. The cerebral cortex was taken from another 6 rats in each group after execution to detect the contents of miR-145 and superoxide dismutase (SOD). RESULTS: Compared with model group, the rats' behavior score was lowered obviously(P<0.05), the infarct volume was markedly decreased(P<0.05),the content of miR-145 was remarkably decreased (P<0.05), and the content of SOD was significantly increased(P<0.05)in the ginsenosides Rb1 group. Compared with ginsenosides Rb1 group, the rats' behavior score was obviously increased (P<0.05), the volume of cerebral infarction was markedly increased(P<0.05), the content of miR-145 was obviously increased (P<0.05), and the content of SOD was significantly decreased (P<0.05) in ginsenosides Rb1+miRNA-145 mimics group. CONCLUSION: Ginsenosides Rb1 can increase the activity of SOD in the brain tissue of rats with cerebral ischemia reperfusion injury by reducing the miRNA-145 content, and protect the brain.

Key words: brain ischemia-reperfusion injury, ginsenoside Rb1, miR-145, superoxide dismutase

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