Abstract
Herein, the structural effect of autologous platelet-rich plasma (PRP) on posttraumatic skeletal muscle regeneration in rats with chronic hyperglycemia (CH) was tested. 130 white laboratory male rats divided into four groups (I—control; II—rats with CH; III—rats with CH and PRP treatment; and IV—rats for CH confirmation) were used for the experiment. CH was simulated by streptozotocin and nicotinic acid administration. Triceps surae muscle injury was reproduced by transverse linear incision. Autologous PRP was used in order to correct the possible negative CH effect on skeletal muscle recovery. On the 28th day after the injury, the regenerating muscle fiber and blood vessel number in the CH+PRP group were higher than those in the CH rats. However, the connective tissue area in the CH group was larger than that in the CH+PRP animals. The amount of agranulocytes in the regenerating muscle of the CH rats was lower compared to that of the CH+PRP group. The histological analysis of skeletal muscle recovery in CH+PRP animals revealed more intensive neoangiogenesis compared to that in the CH group. Herewith, the massive connective tissue development and inflammation signs were observed within the skeletal muscle of CH rats. Obtained results suggest that streptozotocin-induced CH has a negative effect on posttraumatic skeletal muscle regeneration, contributing to massive connective tissue development. The autologous PRP injection promotes muscle recovery process in rats with CH, shifting it away from fibrosis toward the complete muscular organ repair.
Highlights
Skeletal muscle injuries account for about 30% of all occupational diseases in industrialized countries [1]
Jeong et al have shown that myosatellite cells (MSCs) derived from rats with streptozotocin-induced diabetes mellitus (DM) are incapable of myotube formation [8]
All the animals were divided into four groups: I—control group (40 rats with skeletal muscle injury); II—chronic hyperglycemia (CH) group (40 animals with simulated CH and skeletal muscle injury); III—CH+platelet-rich plasma (PRP) group (40 rats with simulated CH and skeletal muscle injury, which received PRP injection into muscle damage area); and IV—CH confirmation group (10 animals with CH for glucose homeostasis evaluation)
Summary
Skeletal muscle injuries account for about 30% of all occupational diseases in industrialized countries [1]. Uncovering the cellular and molecular mechanisms of skeletal muscle regeneration and the development of effective ways of muscle recovery improvement are the important tasks of modern medical science [3]. CH is associated with the development of secondary complications in skeletal muscle and may impair its regeneration capacity. Experimental studies have shown that CH attenuates the expression of muscle-specific transcription factors (MyoD and myogenin) [5] and reduces the number of myosatellite cells (MSCs) in both animal and human skeletal muscle [6, 7]. Jeong et al have shown that MSCs derived from rats with streptozotocin-induced diabetes mellitus (DM) are incapable of myotube formation [8]. Rats with genetic DM models have a significant delay and incompleteness of posttraumatic skeletal muscle regeneration [9, 10]
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