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

Figure 1. Experimental protocol (a) and location of the vagus nerve (b). I/R: ischemia-reperfusion; VNS: vagus nerve stimulation.

Figure 2. VNS alleviates skeletal muscle injury. (a) Control group: normal skeletal muscle cell shape and arrangement; I/R group: skeletal muscle cell degeneration and necrosis, wide range of inflammatory cell accumulation; I/R+VNS group: mixed normal and pathological skeletal muscle cells, little inflammatory cell infiltration. (b) The muscle injury area in the three groups. (c) The serum concentration of CK and LDH. ∗p < 0.05 vs. control group; #p < 0.05 vs. I/R group; HPF: high-power field; CK: creatine kinase; LDH: lactic dehydrogenase.

Figure 3. Effect of VNS on skeletal muscle cell apoptosis. (a) Representative images showing immunofluorescence staining for DAPI (blue) and TUNEL (green) in skeletal muscle cell nuclei from the control, I/R, and I/R+VNS groups. (b) Quantification of skeletal muscle cell apoptosis. ∗p < 0.05 vs. control group; #p < 0.05 vs. I/R group.

Figure 4. VNS mitigates inflammation in SMI/R injury. (a) Relative mRNA levels of IL-1β, IL-6, and TNF-α in the control, I/R, and I/R+VNS groups. (b, c) Representative blots and relative protein expression of IL-1β, IL-6, and TNF-α among different groups. ∗p < 0.05 vs. control group; #p < 0.05 vs. I/R group. IL-1β: interleukin-1β; IL-6: interleukin-6; TNF-α: tumor necrosis factor-α.

Figure 5. VNS attenuates oxidative stress in SMI/R injury. (a-c) The effect of VNS on the MDA, SOD, and MPO levels in skeletal muscle tissues. (d-e) The effect of VNS on the MDA and SOD levels in serum. ∗p < 0.05 vs. control group; #p < 0.05 vs. I/R group. MDA: myeloperoxidase; SOD: superoxide dismutase; MPO: malondialdehyde.

Figure 6. VNS protects vascular endothelial function. (a) Representative examples of eNOS, ICAM-1, and VCAM-1 expression in different groups. (b) Relative expression levels are shown as the ratio between the target proteins and β-actin expression levels. ∗p < 0.05 vs. control group; #p < 0.05 vs. I/R group. eNOS: endothelial nitric oxide synthase; ICAM-1: intercellular cell adhesion molecule-1; VCAM-1: vascular cell adhesion molecule-1.

Figure 7. Schematic diagram depicting the protective effect and potential mechanisms of VNS on SMI/R injury. Noninvasive VNS may become a safe and acceptable technology for treating SMI/R patients.