Abstract

Honey is a natural product rich in several phenolic compounds, enzymes, and sugars with antioxidant, anticarcinogenic, anti-inflammatory, and antimicrobial potential. Indeed, the development of honey-based adhesives for wound care and other biomedical applications are topics being widely investigated over the years. Some of the advantages of the use of honey for wound-healing solutions are the acceleration of dermal repair and epithelialization, angiogenesis promotion, immune response promotion and the reduction in healing-related infections with pathogenic microorganisms. This paper reviews the main role of honey on the development of wound-healing-based applications, the main compounds responsible for the healing capacity, how the honey origin can influence the healing properties, also highlighting promising results in in vitro and in vivo trials. The challenges in the use of honey for wound healing are also covered and discussed. The delivery methodology (direct application, incorporated in fibrous membranes and hydrogels) is also presented and discussed.

Highlights

  • The skin is composed of three layers, and is considered the first physical barrier against external infectious agents

  • The wound-healing process has the purpose of recovering the integrity of the damaged tissue and the regeneration of the epithelium that was lost, and it is a dynamic and complex process that globally occurs in four overlapping steps: hemostasis, inflammation, tissue proliferation, and regeneration [1,2] (Figure 1)

  • This review aims to highlight the mechanism of honey’s action in wound healing and gather the literature available regarding the use of honey and modern engineering templates for promoting modern solutions for wound and skin healing and regeneration

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Summary

Introduction

The skin is composed of three layers (epidermis, dermis, and hypodermis), and is considered the first physical barrier against external infectious agents. Wounds are defined as the disruption in the continuity of the skin, induced by mechanical, chemical, or thermal harms, and resulting in the loss of the defensive functions of this tissue [1]. The cascade of initial vasoconstriction of blood vessels and platelet aggregation play a key role in stopping the loss of blood. The initial vasoconstriction is followed by a vasodilation, which allows an influx of a variety of inflammatory cells which release several types of mediators and cytokines to promote thrombosis, angiogenesis, and reepithelialization. The fibroblasts release extracellular components which initiate the formation of collagen fibers that will serve as scaffolding [1,3]. During the inflammatory phase the hemostasis, chemotaxis, and the increased vascular permeability limit further damage, close the wound, remove cellular debris and bacteria, and promote cellular migration [3].

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