Abstract

To investigate the changes induced by DisBa-01 on repair of wound healing after induced incisional hernia (IH) in rats. Thirty two male albino rats were submitted to IH and divided into four experimental groups: G1, placebo control; G2, DisBa-01-treated; G3, anti-αvβ3 antibodies-treated and G4, anti-α2 antibodies-treated. Histological, biochemical and extracellular matrix remodeling analysis of abdominal wall were evaluated. After 14 days, 100% of the G2 did not present hernia, and the hernia ring was closed by a thin membrane. In contrast, all groups maintained incisional hernia. DisBa-01 also increased the number macrophages and fibroblasts and induced the formation of new vessels. Additionally, MMP-2 was strongly activated only in G2 (p<0.05). Anti- αvβ3-integrin antibodies produced similar results than DisBa-01 but not anti-α2 integrin blocking antibodies. DisBa-01 has an important role in the control of wound healing and the blocking of this integrin may be an interesting therapeutically strategy in incisional hernia.

Highlights

  • Incisional hernias (IH) are usually found as a complication of about 11% of abdominal wall closures

  • DisBa-01 has an important role in the control of wound healing and the blocking of this integrin may be an interesting therapeutically strategy in incisional hernia

  • Β3-integrin deficient mice showed accelerated re-epithelialization associated with enhanced TGF-β1 signaling[18]. These results suggest that the αvβ[3] integrin controls the rate of wound repair, and, it could be a target for new wound healing therapies

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Summary

Introduction

Incisional hernias (IH) are usually found as a complication of about 11% of abdominal wall closures. The distinct phases of wound healing process are well described and include local hemorrhage with extravasation of platelets and platelet-derived growth factors such as PDGF (platelet derived growth factor) and EGF (epidermal growth factor). These mitogens stimulate FGF-7 (fibroblast growth factor-7) expression by fibroblasts. Invading neutrophils and macrophages will secrete several proinflammatory cytokines and growth factors resulting in angiogenesis and fibroplasia. These events will culminate with the synthesis of a provisional matrix that must be able to support the biomechanical forces of the abdominal wall[2]

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