Abstract

Random-pattern skin flap transplantation is frequently applied in plastic and reconstructive surgery. However, the distal part of the flap often suffers necrosis due to ischemia. In this study, the effects of salvianolic acid B (Sal B) on flap survival were evaluated, and the underlying mechanisms were investigated. Sal B improved the survival area, reduced tissue edema, and increased the number of microvessels in skin flaps after 7 days, whereas an autophagy inhibitor (3-methyladenine) reversed the Sal B-induced increase in flap viability. In addition, Sal B stimulated angiogenesis, inhibited apoptosis, reduced oxidative stress, and upregulated autophagy in areas of ischemia. Moreover, the effects of Sal B on angiogenesis, apoptosis, and oxidative stress were reversed by autophagy inhibition. Overall, our findings suggest that Sal B has pro-angiogenesis, anti-apoptosis, and anti-oxidative stress effects by stimulating autophagy, which enhances the survival of random-pattern skin flaps.

Highlights

  • Random-pattern skin flaps are commonly used in plastic surgery to cover skin defects, which are caused by trauma, oncologic resection, or congenital conditions (Tanaka et al, 2003; Harder et al, 2008; Wang et al, 2014; Kanayama et al, 2017)

  • Ischemia and necrosis in the distal part of random skin flaps due to a reduced blood supply are commonly encountered in plastic and reconstructive surgery

  • Our data suggest that salvianolic acid B (Sal B) promotes the survival of random skin flaps by inducing autophagy and angiogenesis, as well as attenuating oxidative stress and apoptosis

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Summary

Introduction

Random-pattern skin flaps are commonly used in plastic surgery to cover skin defects, which are caused by trauma, oncologic resection, or congenital conditions (Tanaka et al, 2003; Harder et al, 2008; Wang et al, 2014; Kanayama et al, 2017). Sal B Promotes Skin Flaps Survival angiogenesis (Stell, 1976). Angiogenesis is infrequent in the distal part of the flap (Saito et al, 2018). After vascular regeneration in a cutaneous flap, reperfusion and restoration of blood supply result in IRI by promoting necrosis (Lin et al, 2017). Oxidative stress and apoptosis are two major mechanisms of IRI and are key factors in the necrosis of random-pattern flaps (Deheng et al, 2016). Ischemic necrosis of random skin flaps can be ameliorated by promoting angiogenesis and inhibiting oxidative stress and apoptosis

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