Journal of Immunology Research (Jan 2020)

Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury

  • Lanqing Meng,
  • Qing Huang,
  • Xuebin Li,
  • Ping Liang,
  • Yueyong Li,
  • Xiaohua Huang,
  • Jingjie Zhao,
  • Qiuping Chen,
  • Rong Qiu,
  • Lan Li,
  • Chongdong Jian,
  • Hongfei Yao,
  • Jianmin Huang,
  • Xionglin Tang,
  • Zechen Wang,
  • Zhongheng Wei,
  • Jun Wu,
  • Liuzhi Wei,
  • Qiuju Wei,
  • Qianli Tang,
  • Lu Huang,
  • Jihua Wei,
  • Dinggui Lu,
  • Qunqiang Luo,
  • Kegong Xie,
  • Yang Ouyang,
  • Jian Chen,
  • Genliang Li,
  • Linxue Luo,
  • Linbo He,
  • Chenyi Zhuo,
  • Anding Xu,
  • Lingzhang Meng

DOI
https://doi.org/10.1155/2020/8873261
Journal volume & issue
Vol. 2020

Abstract

Read online

Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN’s neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.