Neuropsychiatric Disease and Treatment (Mar 2021)

Vagal Nerve Stimulation Protects Against Cerebral Ischemia–Reperfusion Injury in Rats by Inhibiting Autophagy and Apoptosis

  • Zhang LN,
  • Zhang XW,
  • Li CQ,
  • Guo J,
  • Chen YP,
  • Chen SL

Journal volume & issue
Vol. Volume 17
pp. 905 – 913

Abstract

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Li-Na Zhang,1,* Xian-Wei Zhang,1,* Chang-Qing Li,2 Jing Guo,1 Yong-Ping Chen,1 Sheng-Li Chen1 1Department of Neurology, Chongqing University Three Gorges Hospital, Chongqing, 404000, People’s Republic of China; 2Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, People’s Republic of China*These authors contributed equally to this workCorrespondence: Sheng-Li ChenDepartment of Neurology, Chongqing University Three Gorges Hospital, Number 165 Xincheng Road, Wanzhou District, Chongqing, 404000, People’s Republic of ChinaTel +86 58103452Fax +86 58103668Email [email protected]: Cumulative evidence suggests that neuronal death including autophagy, apoptosis, and necrosis is closely related to the occurrence and development of cerebral ischemia–reperfusion (I/R) injury. Moreover, vagal nerve stimulation (VNS) is involved in many different neuroprotective and neuroplasticity pathways. Thus, VNS may be a novel approach for treating various neurodegenerative diseases. The present study aims to determine whether VNS protects against cerebral I/R injury in rats by inhibiting autophagy and apoptosis.Methods: Cerebral I/R injury is induced by middle cerebral artery occlusion (MCAO) and VNS is carried out. Infarct volume, neurological deficit, autophagy, and apoptosis are examined 24 h after reperfusion.Results: Vagal nerve stimulation decreases infarct volume and suppresses neurological deficit. Moreover, obvious autophagy and apoptosis are detected in rats that have undergone I/R, and VNS inhibits autophagy and apoptosis.Conclusion: Vagal nerve stimulation exerts neuroprotective effects following I/R injury by inhibiting autophagy and apoptosis.Keywords: vagal nerve stimulation, cerebral ischemia–reperfusion injury, autophagy, apoptosis

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