Abstract
Refractory diabetic foot ulcer is commonly encountered in clinical practice and it is hardly cured with a long duration of treatment and a high expense, as such problem involves multiple disciplines. Therefore, in case of refractory wounds, it is necessary to first analyze the causes, general or local. Immunohistochemistry (IHC) was conducted to determine α-SMA, chemokines 12 (CXCL12) and chemokines 4 (CXCR4) levels in pancreatic tissues and distant normal pancreatic tissues. Cells were treated with recombinant human CXCL12 (rhCXCL12) or the CXCR4 antagonist AMD3100. After treatment, Western blot determined FAK-AKT and ERK1/2 expression in islet cells, whilst ELISA detected the content of IL-6 and IL-8. rhCXCL12 increased the expression and secretion of Interleukin-6 (IL-6) time- and dose-dependently. But the advent of CXCR4 antagonist abrogated the protective effect of rhCXCL12. rhCXCL12 exhibited a protective effect on apoptosis, but this effect was abrogated by down-regulation of IL-6 with AMD3100. In addition, rhCXCL12 increased the phosphorylation of FAK, ERK1/2, AKT, and P38 and inhibition of FAK inhibited IL-6 expression. FAK inhibition almost completely blocked CXCL12-induced activation. This study demonstrates that CXCL12/CXCR4 pathway mediates the expression of IL-6 to enhance healing of refractory diabetic foot wounds by down-regulating the FAK pathway.
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