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Oxidative Medicine and Cellular Longevity
Volume 2019, Article ID 9208949, 10 pages
https://doi.org/10.1155/2019/9208949
Research Article

Vagus Nerve Stimulation Attenuates Acute Skeletal Muscle Injury Induced by Ischemia-Reperfusion in Rats

1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Wuhan 430060, China
4Department of Orthopedics, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430077, China
5Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

Correspondence should be addressed to Shengli Yang; moc.oohay@4102ilgnehsgnay and Hong Jiang; moc.361@gnohgnaijuhw

Received 17 September 2018; Revised 3 December 2018; Accepted 18 December 2018; Published 28 February 2019

Guest Editor: Carine Smith

Copyright © 2019 Yifeng Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 ( 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.