中国药物警戒 ›› 2023, Vol. 20 ›› Issue (4): 454-459.
DOI: 10.19803/j.1672-8629.20220269

• 安全与合理用药 • 上一篇    下一篇

基于生物信息学探讨三七对脑缺血再灌注损伤大鼠基因表达的影响

刘洁1, 刘胜伟2, 任忠洋3, 丁玲1, 陈昶2, 胡毅1,*   

  1. 1重庆市江津区中心医院,重庆 402260;
    2重庆医科大学附属永川医院,重庆 402160;
    3重庆市江津区中医院,重庆 402284
  • 收稿日期:2022-05-24 出版日期:2023-04-15 发布日期:2023-04-20
  • 通讯作者: *胡毅,男,本科,副主任医师,内科学与生物信息学。E-mail：965378674@qq.com
  • 作者简介:刘洁,女,硕士,主管药师,生物信息学与中药药理。
  • 基金资助:
    重庆市自然科学基金资助项目（cstc2020jcyj-msxmX0434）; 重庆市科卫联合医学科研基金资助项目（2021MSXM104）; 学科经费资助：重庆市临床药学重点学科

Effects of Panax notoginseng on gene expressions in rats with cerebral ischemia-reperfusion injury based on bioinformatics

LIU Jie1, LIU Shengwei2, REN Zhongyang3, DING Ling1, CHEN Chang2, HU Yi1,*   

  1. 1Jiangjin Central Hospital of Chongqing, Chongqing 402260, China;
    2Yongchuan Hospital of Chongqing Medical University, Chongqing 402160, China;
    3Jiangjin Hospital of Traditional Chinese Medicine, Chongqing 402284, China
  • Received:2022-05-24 Online:2023-04-15 Published:2023-04-20

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摘要： 目的 基于生物信息学预测三七（Panax notoginseng）抗脑缺血再灌注损伤（cerebral ischemia reperfusion injury, CIRI）可能作用靶点及其信号通路。方法 通过 GEO 数据库,获取包含大脑中动脉阻塞（middle cerebral artery occlusion,MCAO）大鼠模型组（简称“MCAO大鼠模型组”）、三七实验组大脑皮层的基因检测结果,筛选关键差异基因,然后进行GO 富集与 KEGG 通路分析,探讨三七抗脑缺血再灌注损伤可能的分子机制。结果 筛选出 444个差异 mRNA,关键差异基因为Fn1、Gsk3b、Snap25等;通过KEGG富集通路分析得到20条显著通路,结合脑缺血再灌注损伤机制与相关文献检索报道,关键通路为Rap1信号通路、cAMP信号通路、自噬信号通路、AMPK信号通路等,其中在MCAO大鼠模型中,三七与自噬通路的相关研究尚少;也尚未查到三七单药关于Gsk3b、Snap25靶点的研究。结论 在脑缺血再灌注损伤中,三七可能从抗炎、抗氧化、抗凋亡、自噬等方面发挥一定的保护作用,为三七深入研究奠定了基础。

关键词: 三七, 脑缺血再灌注, 生物信息学, 差异基因, 大鼠, 基因表达

Abstract: Objective To predict the possible targets and signaling pathways involved in anti-cerebral ischemia/reperfusion injury by Panax Notoginseng (PN) based on bioinformatics. Methods Gene expressions in the cerebral cortex of the middle cerebral artery occlusion (MCAO) model group and the Panax notoginseng (PN) drug delivery group of rats were obtained from the GEO database. The key differentially expressed genes (DEGs) were screened before GO enrichment and KEGG pathway analyses were performed to explore the possible molecular mechanisms by which Panax notoginseng combated cerebral ischemia/reperfusion injury. Results Four hundred and forty-four differential mRNAs were screened, and the key DEGs were Fn1, Gsk3b and Snap25. Twenty significant pathways were obtained after KEGG enrichment pathway analysis. Based on the mechanism for cerebral ischemia/ reperfusion injury and related literature, the key pathways were found to be to Rap1 signaling pathway, cAMP signal pathway, autophagy signal pathway, and AMPK signal pathway. There have been few studies related to Panax notoginseng and autophagy pathways on the MCAO rat model. No studies have been found on Panax notoginseng related targets of Gsk3b and Snap25. Conclusion Panax notoginseng may protect against cerebral ischemia / reperfusion injury by combating inflammation, oxidation, apoptosis or via autophagy.

Key words: Panax notoginseng, cerebral ischemia-reperfusion injury, bioinformatics, differentially expressed genes, rats, gene expression

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