Myoprotective effects of bFGF on skeletal muscle injury in pressure-related deep tissue injury in rats. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Shi, Hongxue; Xie, Haohuang; Zhao, Yan; Lin, Cai; Cui, Feifei; Pan, Yingying; Wang, Xiaohui; Zhu, Jingjing; Cai, Pingtao; Zhang, Hongyu; Fu, Xiaobing; Xiao, Jian; Jiang, Liping
• Is Part Of: Burns and trauma. Volume 4:Issue 1(2016)
• Page Start: 1
• Page End: 10
• Publication Date: 2016-12
• Subjects: Pressure ulcer -- Skeletal muscle injury -- bFGF -- Regeneration -- PI3K/Akt/mTOR; Burns and scalds -- Periodicals; Wounds and injuries -- Periodicals; 617.11
• DOI: 10.1186/s41038-016-0051-y
• Languages: English
• ISSNs: 2321-3876

Abstract

Abstract Background Pressure ulcers (PUs) are a major clinical problem that constitutes a tremendous economic burden on healthcare systems. Deep tissue injury (DTI) is a unique serious type of pressure ulcer that arises in skeletal muscle tissue. DTI arises in part because skeletal muscle tissues are more susceptible than skin to external compression. Unfortunately, few effective therapies are currently available for muscle injury. Basic fibroblast growth factor (bFGF), a potent mitogen and survival factor for various cells, plays a crucial role in the regulation of muscle development and homeostasis. The main purpose of this study was to test whether local administration of bFGF could accelerate muscle regeneration in a rat DTI model. Methods Male Sprague Dawley (SD) rats (age 12 weeks) were individually housed in plastic cages and a DTI PU model was induced according to methods described before. Animals were randomly divided into three groups: a normal group, a PU group treated with saline, and a PU group treated with bFGF (10 μg/0.1 ml) subcutaneously near the wound. Results We found that application of bFGF accelerated the rate of wound closure and promoted cell proliferation and tissue angiogenesis. In addition, compared to saline administration, bFGF treatment prevented collagen deposition, a measure of fibrosis, and up-regulated the myogenic marker proteins MyHC and myogenin, suggesting bFGF promoted injured muscle regeneration. Moreover, bFGF treatment increased levels of myogenesis-related proteins p-Akt and p-mTOR. Conclusions Our findings show that bFGF accelerated injured skeletal muscle regeneration through activation of the PI3K/Akt/mTOR signaling pathway and suggest that administration of bFGF is a potential therapeutic strategy for the treatment of skeletal muscle injury in PUs.