Abstract
BackgroundThe mechanisms of muscle injury repair after EPI® technique, a treatment based on electrical stimulation, have not been described. This study determines whether EPI® therapy could improve muscle damage.MethodsTwenty-four rats were divided into a control group, Notexin group (7 and 14 days) and a Notexin + EPI group. To induce muscle injury, Notexin was injected in the quadriceps of the left extremity of rats. Pro-inflammatory interleukin 1-beta (IL-1beta) and tumoral necrosis factor-alpha (TNF-alpha) were determined by ELISA. The expression of receptor peroxisome gamma proliferator activator (PPAR-gamma), vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor-1 (VEGF-R1) were determined by western-blot.ResultsThe plasma levels of TNF-alpha and IL-1beta in Notexin-injured rats showed a significant increase compared with the control group. EPI® produced a return of TNF-alpha and IL-1beta values to control levels. PPAR-gamma expression diminished injured quadriceps muscle in rats. EPI® increased PPAR-gamma, VEGF and VEGF-R1 expressions. EPI® decreased plasma levels of pro-inflammatory TNF-alpha and IL-1beta and increased anti-inflammatory PPAR-gamma and proangiogenic factors as well as VEGF and VEGF-R1 expressions.ConclusionThe EPI® technique may affect inflammatory mediators in damaged muscle tissue and influences the new vascularization of the injured area. These results suggest that EPI® might represent a useful new therapy for the treatment of muscle injuries. Although our study in rats may represent a valid approach to evaluate EPI® treatment, studies designed to determine how the EPI® treatment may affect recovery of injury in humans are needed.
Highlights
The mechanisms of muscle injury repair after EPI® technique, a treatment based on electrical stimulation, have not been described
Notexin produced tissue injury characterized as an anechoic ultrasound image with fluid collection corresponding to a muscle lesion (Figure 2A)
The main findings of this study is that EPI® applied after Notexin-induced muscle injury in rats decreases the production of the inflammatory mediators tumor necrosis factor-α (TNF-α) and IL1β, increases the protein expression of anti-inflammatory factor PPAR-γ and the angiogenic involved proteins vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor-1 (VEGF-R1)
Summary
The mechanisms of muscle injury repair after EPI® technique, a treatment based on electrical stimulation, have not been described. This study determines whether EPI® therapy could improve muscle damage. Soft tissue injuries are recurrent in sports and have an incidence rate of some 30% [1]. Abat et al BMC Sports Science, Medicine, and Rehabilitation (2015) 7:7 vasodilatation induced by two mechanisms comes about through the release of histamines from the cells present within the damaged area and by activating the route of the vascular endothelial growth factor and nitric oxide (VEGF-NO) [8]. VEGF is the most important capillary growth factor in skeletal muscle [7] and is essential to basal capillarization in the tissue and increased capillary growth in response to different mechanical stimuli [9]
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