Abstract
The present study aimed to evaluate the effect of natural hirudin on rat random skin flap viability and to determine the mechanism. Forty-eight rats were randomly divided into 2 groups. After the dorsal skin flap operation (3 cm × 10 cm in size), subcutaneous injections of 6 ATU hirudin were administered to group H (n = 24) every 12 h, while group C (n = 24) received an equal volume of 0.9% normal saline. Six rats from each group were euthanized 1, 2, 4, and 7 days after the operation. A full skin sample was collected from these rats to measure the p38-mitogen-activated protein kinase (p38-MAPK), phospho-p38- (Pp38-) MAPK, nuclear factor-κB (NF-κB) p65, phosphor-NF-κB (pNF-κB) p65, tumour necrosis factor- (TNF-) α, interleukin- (IL-) 6, and intercellular adhesion molecule- (ICAM-) 1 levels via western blot (WB) assays. The results showed that flap viability was significantly higher in the hirudin-treated group, which showed a reduced inflammatory response compared with the control group. The Pp38/p38, pNF-κB p65/NF-κB p65, TNF-α, IL-6, and ICAM-1 levels in the hirudin-treated group were lower than those in the control group. The results demonstrated that hirudin could improve random skin flap viability and suggested that this effect maybe occurs by blocking the thrombin/proteinase-activated receptors (PARs)/p38/NF-κB signalling pathway, thus decreasing the inflammatory response.
Highlights
Random pattern skin flaps are commonly used to repair skin defects during plastic and reconstructive surgery, flap necrosis remains a problem
We applied the same model in our study and found that the areas of flap necrosis in group C were similar to those in the control groups used in other studies
The results of this study showed that the p38-MAPK and nuclear factor-κB (NF-κB) levels in flaps from group C were significantly increased 2 days after surgery, which is consistent with the above hypothesis
Summary
Random pattern skin flaps are commonly used to repair skin defects during plastic and reconstructive surgery, flap necrosis remains a problem Many medications, such as sympatholytics, vasodilators, calcium channel blockers, prostaglandin inhibitors, glucocorticoids, and free radical scavengers, have been reported to be effective for increasing flap viability [1, 2]. These drugs cannot entirely prevent flap necrosis. The aim of the present study was to evaluate the effect of hirudin on inflammation in rat random pattern skin flaps and to explore its underlying mechanism
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