Abstract
Ischemic stroke is the leading cause of death and disability. Microglia are polarized toward the proinflammatory M1 phenotype and neuroprotective M2 phenotype after stroke and play an important role in the pathological process of ischemic stroke. Emerging research suggests that vagus nerve stimulation (VNS) can mediate microglia polarization after ischemic stroke and may serve as a potential treatment for ischemic stroke. However, the mechanism by which VNS mediates microglia polarization remains unclear. In this study, we aimed to investigate the underlying mechanism. Sprague-Dawley rats were randomly divided into the sham, ischemic stroke, ischemic stroke + VNS, ischemic stroke + VNS + lentivirus (LV)-TLR4 and ischemic stroke + VNS + LV-CON groups. LV was injected into the lateral ventricles of the rats 14 days before ischemic stroke surgery, and VNS was administered after 30 min of occlusion. We assessed the infarct volume, neurological scores, the TLR4/MyD88/NF-κB protein level and microglia polarization after 3 days of reperfusion. Our results revealed that VNS can promote M2 microglia polarization and inhibit M1 microglia polarization to alleviate brain injury via inhibition of the TLR4/MyD88/NF-κB pathway in microglia in the acute stage of stroke.
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