Vagus nerve stimulation attenuates @entity2806 and reperfusion injury via endogenous cholinergic pathway in XXXX .

@entity32 @entity2308 @entity2806 @entity63 @entity5698 @entity1977 @entity1188 @entity35 @entity385 @entity934
@entity32 and apoptosis play critical roles in the acute progression of @entity63 pathology. Emerging evidence indicates that vagus nerve stimulation (VNS) following focal @entity2806 and reperfusion (I/R) may be neuroprotective by limiting @entity1188 size. However, the underlying molecular mechanisms remain unclear. In this study, we investigated whether the protective effects of VNS in acute cerebral I/R injury were associated with anti-inflammatory and anti-apoptotic processes. Male Sprague-Dawley (SD) @entity35 underwent VNS at 30 min after focal cerebral I/R surgery. Twenty-four h after reperfusion, neurological deficit scores, @entity1188 volume, and neuronal apoptosis were evaluated. In addition, the levels of pro-inflammatory cytokines were detected using enzyme-linked immune sorbent assay (ELISA), and immunofluorescence staining for the endogenous "cholinergic anti-inflammatory pathway" was also performed. The protein expression of a7 nicotinic @entity934 receptor (a7nAchR), phosphorylated @entity2308 (p- @entity2308 ), and cleaved caspase 3 in @entity63 penumbra were determined with Western blot analysis. I/ @entity5698 treated with VNS (I/R+VNS) had significantly better neurological deficit scores, reduced @entity385 , and decreased number of TdT mediated @entity1977 nick end labeling (TUNEL) positive cells. Furthermore, in the @entity63 penumbra of the I/R+VNS group, the levels of pro-inflammatory cytokines and cleaved caspase 3 protein were significantly decreased, and the levels of a7nAchR and phosphorylated @entity2308 were significantly increased relative to the I/R alone group. These results indicate that VNS is neuroprotective in acute cerebral I/R injury by suppressing @entity32 and apoptosis via activation of cholinergic and a7nAchR/ @entity2308 pathways.
