Background: 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.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8008252 | PMC |
http://dx.doi.org/10.2147/NDT.S300535 | DOI Listing |
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