1000 Section - Exploring the effects of vagus nerve stimulation on ischemia-reperfusion rats based on transcriptomics and DIA proteomics

Wednesday, May 20, 2026

6:00 PM - 7:30 PM PT

Presenting Author/Autor expositor(s)

KC

Keling Cheng, PhD

PhD
福建医科大学附属第一医院
Fuzhou, Fujian, China (People's Republic)

Co-Author/Coautor(s)

BW

Bin Wang, PhD

PhD
福建医科大学附属第一医院
Fuzhou, Fujian, China (People's Republic)
ZW

Zhiyong Wang, PhD

PhD
福建医科大学附属第一医院
Fuzhou, Fujian, China (People's Republic)

Corresponding Author/Autor a quien dirigir la corr(s)

JN

Jun Ni, PhD

PhD
福建医科大学附属第一医院
Fuzhou, Fujian, China (People's Republic)

Objectives : In cerebral ischemia/reperfusion injury (I/R) rat model, VNS exerts neuroprotective effects by ameliorating neurological injury and inhibiting neuroinflammation and apoptosis. However, the underlying molecular mechanisms and biological processes for the amelioration of I/R injury mediated by VNS remain ambiguous. We aim to clarify the therapeutic effect of VNS in I/R rats and to investigate the potential molecular targets and mechanisms of VNS by using transcriptomics and DIA proteomics.

Design: We established I/R rat and administered VNS intervention on I/R rat for 7 days, after which the neurological deficits and water/food intake of the rats were detected, and the therapeutic effect of VNS in I/R rats evaluated by Hematoxylin-Eosin staining, immunohistochemistry, immunofluorescence methods. We further explored the potential biological processes and molecular mechanisms of VNS in I/R rats using transcriptomics and DIA proteomics, and validated potential targets by qRT-PCR

Results: Our research confirms that VNS alleviated neurological deficits and improved water/food intake while also inhibiting cell apoptosis and promoting cell proliferation. Addtionally, the neuroprotective effect mediated by VNS is closely related to key targets such as Lrg1, Sulta1a1, and Fkbp5.

Conclusion: Our results showed the positive effects of VNS intervention in improving the function of neurological deficits in rats with I/R loss at the behavioral, pathological, and molecular levels, and Lrg1, Fkbp5, and Sult1a1 may be associated with VNS intervention effects and are potentially explorable key targets.