An experimental study of muscular injury repair in a mouse model of notexin-induced lesion with EPI® technique

Abstract

Background: 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. Methods: Twenty-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. Results: The 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. Conclusion: The EPI® techniquemay 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.