Background: The mechanisms of muscle injury repair after EPI�® technique, a treatment based on electrical\nstimulation, have not been described. This study determines whether EPI�® therapy could improve muscle damage.\nMethods: Twenty-four rats were divided into a control group, Notexin group (7 and 14 days) and a Notexin + EPI group.\nTo induce muscle injury, Notexin was injected in the quadriceps of the left extremity of rats. Pro-inflammatory interleukin\n1-beta (IL-1beta) and tumoral necrosis factor-alpha (TNF-alpha) were determined by ELISA. The expression of receptor\nperoxisome gamma proliferator activator (PPAR-gamma), vascular endothelial growth factor (VEGF) and vascular\nendothelial growth factor receptor-1 (VEGF-R1) were determined by western-blot.\nResults: The plasma levels of TNF-alpha and IL-1beta in Notexin-injured rats showed a significant increase compared\nwith the control group. EPI�® produced a return of TNF-alpha and IL-1beta values to control levels. PPAR-gamma\nexpression diminished injured quadriceps muscle in rats. EPI�® increased PPAR-gamma, VEGF and VEGF-R1 expressions.\nEPI�® decreased plasma levels of pro-inflammatory TNF-alpha and IL-1beta and increased anti-inflammatory PPAR-gamma\nand proangiogenic factors as well as VEGF and VEGF-R1 expressions.\nConclusion: The EPI�® technique may affect inflammatory mediators in damaged muscle tissue and influences the new\nvascularization of the injured area. These results suggest that EPI�® might represent a useful new therapy for the treatment\nof muscle injuries. Although our study in rats may represent a valid approach to evaluate EPI�® treatment, studies designed\nto determine how the EPI�® treatment may affect recovery of injury in humans are needed.
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