The protective effect of Irisin against ischemia-reperfusion injury after perforator flap grafting in rats

Publication date: Available online 28 September 2018

Source: Injury

Author(s): Gang Zhao, Xin Zhang, Peng Xu, Jing-Yi Mi, Yong-Jun Rui

Abstract

Background

Ischemia-reperfusion injury is one of the reasons for failure of flap grafting. In the present study, we investigated the protective effect of irisin on the survival of perforator flaps in rats.

Methods

A total of 48 adult Sprague-Dawley rats were divided into 2 groups and subjected to vascular clipping of perforator flap. Rats in the experimental group (n = 24) received daily tail intravenous injection of irisin (2 ng/g) for 3 days, while the rest rats in the control group (n = 24) received injection of saline solution of the same dose. On the 7th post-operative day, the surviving area of the flaps were recorded as the percentage of the total flap area. Histology study with haematoxylin and eosin staining were performed in all flaps. Flaps were also evaluated with lead oxide-gelatine-enhanced flap angiography. Immunohistochemical study was performed to evaluate the expression of ErG, a marker of vascular endothelial cells. The tissue of "choke vessels" was excised for quantification of p-Akt/Akt by western blot assay on the 7th post-operative day.

Results

On the 7th post-operative day, the percentage of surviving flap area was significantly larger in the rats with irisin administration (experimental group), compared with the control group (P = 0.011). The density of microvessels was significantly higher in the experimental group (P = 0.03) in the histological study and angiography, with a higher expression level of ErG in the immunochemical study (P = 0.01). The p-Akt/Akt was also higher in the experimental group in Western blotting analysis (P < 0.001).

Conclusion

Irisin has a beneficial effect on protecting perforator flaps from ischemic-reperfusion injury following the flap grafting surgery. It was potentially achieved by promoting proliferation of vascular endothelial cells after flap revascularization. Upregulation of the PI3K/Akt signaling pathway was potentially related with this process.

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