Abstract

Vagus nerve stimulation (VNS) has been shown to attenuate ischemia-reperfusion (I/R) injury in multiple organs. The present study aimed at investigating whether VNS could exert protective effects against I/R injury in the skeletal muscle. Male Sprague-Dawley rats were randomly divided into 3 groups: the control, I/R, and I/R+VNS groups. The skeletal muscle I/R (SMI/R) model was induced by occlusion of the left femoral artery for 2.5 hours followed by reperfusion for 2 hours. The vagal nerve trunk was separated, and VNS was performed during the whole I/R process. The intensity of VNS was optimized in each rat to obtain a 10% reduction in the heart rate relative to the value before stimulation. After the experiment, the blood sample and left gastrocnemius muscle tissues were collected for histological examination, biochemical analysis, and molecular biological detection. During the I/R process, VNS significantly reduced cellular apoptosis, necrosis, and inflammatory cell infiltration compared to sham VNS. The VNS treatment also decreased the inflammatory response, alleviated oxidative stress, and improved vascular endothelial function (p < 0.05 for each). In contrast, the I/R group showed an opposite effect compared to the control group. The present study indicated that VNS could protect against SMI/R injury by suppressing excessive inflammation, alleviating oxidative stress, and preserving vascular endothelial function.

Highlights

  • Skeletal muscle ischemia-reperfusion (SMI/R) injury is a common disease in clinical practice

  • Numerous studies have demonstrated that the pathogenesis of SMI/R injury is associated with inflammation responses and oxidative stress [3]

  • In the present study, using an acute SMI/R model in rats, we aimed to demonstrate the protective effects of Vagus nerve stimulation (VNS) against SMI/R injury and further explore the potential mechanisms

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Summary

Introduction

Skeletal muscle ischemia-reperfusion (SMI/R) injury is a common disease in clinical practice. It often influences the function of the skeletal muscle and can even be life-threatening [1]. Numerous studies have demonstrated that the pathogenesis of SMI/R injury is associated with inflammation responses and oxidative stress [3]. Our clinical study has shown that transcutaneous VNS can markedly attenuate myocardial I/R injury in acute myocardial infarction patients undergoing primary percutaneous coronary intervention [10]. The protective effects of VNS against SMI/R injury remain unknown. In the present study, using an acute SMI/R model in rats, we aimed to demonstrate the protective effects of VNS against SMI/R injury and further explore the potential mechanisms

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