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BMC Sports Sci Med Rehabil. 2015 Apr 17;7:7. doi: 10.1186/s13102-015-0002-0. eCollection 2015.

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

Author information

1
Department of Sports Orthopedics, ReSport Clinic, Barcelona, Spain.
2
Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain.
3
Catalan Institut of Traumatology and Sports Medicine (ICATME), Hospital Universitari Dexeus, Universitat Autónoma de Barcelona, Barcelona, Spain ; Department of Orthopedic Surgery, Hospital de la Santa Creu i Sant Pau, University Autonoma of Barcelona, Barcelona, Spain.
4
Department of Sports Rehabilitation, Cerede Sports Medicine, Barcelona, Spain.
5
Catalan Institut of Traumatology and Sports Medicine (ICATME), Hospital Universitari Dexeus, Universitat Autónoma de Barcelona, Barcelona, Spain ; Universitat Autónoma de Barcelona, Barcelona, Spain ; Department of Orthopedic Surgery and Traumatology, Hospital del Mar, Universitat Autónoma de Barcelona, Barcelona, Spain.

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® 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.

KEYWORDS:

EPI; Injury; Muscle; Notexin-induced; Technique

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