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The skin is an organ that covers the external surface of the body and protects it from exterior hazards. This organ includes the skin and its derivatives such as skin glands (oil glands and sweat glands), hair, nails, and breast. Anatomically, from exterior to interior the skin includes three layers which are called: epidermis, dermis, and hypodermis (or the subcutaneous oil tissues).1 The wound is defined as tissue rupture and/or local destruction of epidermis and dermis which eventually results in the remaining scar. Healing includes two steps: (1) contraction and (2) replacement of the destroyed tissue which occurs via cell transfer and division of alongside cells.2, 3 First, a temporary arteriole contraction occurs and afterward the vessels dilate. Neutrophils initiate adhesion to blood vessel walls and vessel permeability increases. Leukocytes and few lymphocytes appear and glycoprotein networks surround them during the first 3 h.4–6 The number of neutrophils in wound increases during the first 48 h. Few monocytes appear in the first 24 h, and then increase in the following days. Macrophages increase gradually along with neutrophil number reduction. Macrophages produce fibroblast growth factors as well as factors responsible for new vessel production. Blood coagulation is the first healing signal.7 Fibrinopeptide and thrombin attract the macrophages to the damaged tissue and the activated platelets secrete PDGF, IGF-1, and TGFβ which all prepare the target cells for proliferation. Subsequently, fibrin stimulates the macrophages to secrete more healing signals.8 When damaged endothelial cells secrete cytokines, integrin and its receptor appear on the surface of passing leukocytes and inflammation begins. Newcomer inflammatory cells increase the metabolic need.9 Since the local microvascular construction is damaged, energy and O2 reduction, and CO2 and lactate accumulation occur at the damaged site. These happenings initiate the healing process and reassure its maintenance.10 In wounds that are initially sewed, the branched vessels quickly join the branched vessel from the front and the blood circulation of the wound is established.12 In remaining or not fully closed wounds, the new vessels only join the neighbor vessels on the same side of the wound and the granulation tissue is created instead.13 Angiogenesis is inducible by the addition of chemotactic substances to the endothelial cells in the tissue body of the wound. It seems that wound angiogenesis is a response to local energy reduction and its general mechanism is very similar to the mechanism of collagen sediment regulation.11 In unsuitable conditions (hypoxia or lactate increasing), macrophages secrete a chemotactic peptide for endothelial cells which leads to angiogenesis.14 NAD+ reserve protection inhibits this process drastically. Therefore, the unanswered metabolic needs cause an anatomical response with means of a series of growth factors that probably have high importance.15 This step starts approximately from Day 4 or 5. During healing, fibroplasia (fibroblast proliferation) is stimulated from various mechanisms that start with secretion of PDFG, IGF-1, and TGFβ from platelets and resumes with the secretion of cytokines from the macrophage.16 Fibroblasts secrete IGF-1. Epidermal growth and GF1 are also transferred to the damage site via blood circulation. Healing fibroblasts are mostly seen near the wound edges.17 At this place, an appropriate growth environment and oxygen pressure close to 40 mmHg are available for them in normal wounds.18 Investigating the healing effect of the hydroalcoholic extract of pomegranate seed (Punica granatum) on the full thickness wound in rabbit Ali Asghar Hemmati1, Iran Rashidi2, Sedigheh Dahanzadeh1, Mahmoud Moeini1