Chemical burns take up a high proportion of
burns admissions and can penetrate deep into tissues. Various
reagents have been applied in the treatment of skin
chemical burns; however, no optimal
reagent for skin
chemical burns currently exists. The present study investigated the effect of topical body protective compound (BPC)-157 treatment on skin wound healing, using an
alkali burn rat model. Topical treatment with
BPC-157 was shown to accelerate
wound closure following an
alkali burn. Histological examination of skin sections with
hematoxylin-
eosin and Masson staining showed better granulation tissue formation, reepithelialization, dermal remodeling, and a higher extent of
collagen deposition when compared to the model control group on the 18th day postwounding.
BPC-157 could promote
vascular endothelial growth factor expression in wounded skin tissues. Furthermore,
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and cell cycle analysis demonstrated that
BPC-157 enhanced the proliferation of human umbilical vein endothelial cells (HUVECs). Transwell assay and wound healing assay showed that
BPC-157 significantly promoted migration of HUVECs. We also observed that
BPC-157 upregulated the expression of
VEGF-a and accelerated vascular tube formation in vitro. Moreover, further studies suggested that
BPC-157 regulated the phosphorylation level of
extracellular signal-regulated kinases 1 and 2 (ERK1/2) as well as its downstream targets, including c-Fos, c-Jun, and Egr-1, which are key molecules involved in cell growth, migration, and angiogenesis. Altogether, our results indicated that
BPC-157 treatment may accelerate wound healing in a model of
alkali burn-induced skin injury. The therapeutic mechanism may be associated with accelerated granulation tissue formation, reepithelialization, dermal remodeling, and
collagen deposition through ERK1/2 signaling pathway.