Prolonged wound healing is a complication that contributes to morbidity and mortality. Overweight people regularly undergo surgery and trauma, and often develop chronic wounds, but the effects of the adipose tissue excess on cutaneous wound healing are not well understood. This study tested the hypothesis that overweight induced by a high-fat diet impairs rat cutaneous wound healing. Male Wistar rats were fed with either a high-fat or a standard (control) diet. After 15 weeks, an excisional lesion was done and the animals were killed 21 d later. Wound contraction and re-epithelialization, blood pressure, glucose and retroperitoneal fat were evaluated. After killing, lesion and adjacent normal skin were formol-fixed and paraffin-embedded. Inflammatory infiltrate, myofibroblasts, collagen fibres and cellular proliferation were analysed and blood vessels were evaluated using stereological methods. There was no difference in blood pressure and glucose, but retroperitoneal fat increased in the high-fat diet group. Animals fed with the high-fat diet presented delayed wound contraction and re-epithelialization. It was found that 21 d after wounding, overweight induced by a high-fat diet increased the inflammatory infiltrate and delayed myofibroblastic differentiation, collagen deposition, epithelial and connective tissue cell proliferation, and angiogenesis. These findings support the hypothesis that a high-fat diet exerts negative effects on rat cutaneous wound healing, due mainly to the prolongation of the inflammatory phase.
Sympathetic nerve failure has been proposed as a contributing factor in impaired cutaneous wound healing in diabetes mellitus. Nevertheless, no studies have shown whether beta-adrenoceptor blockade through beta-blocker (e.g., propranolol) administration may alter healing of diabetic cutaneous lesions. This study evaluated macro- and microscopically the effects of propranolol administration on cutaneous wound healing in streptozotocin-induced diabetic rats. Acute diabetes was induced by a single intraperitoneal injection of streptozotocin 14 days before wounding. Animals were treated with propranolol (50 mg/kg) dissolved in drinking water; controls received water only. Administration of beta-receptor antagonist began 1 day before wounding and was continued daily until euthanasia. A full-thickness excisional lesion (1 cm(2)) was created. The wound area was measured weekly and the animals were killed 14 days after wounding. Lesions and adjacent skin were formalin-fixed and paraffin-embedded. Sections were stained with hematoxylin-eosin, Sirius red, and toluidine blue, and immunostained for CD-68, alpha-smooth muscle actin and proliferating cell nuclear antigen. The wound area was significantly smaller in the propranolol-treated group than in the control group 7 and 14 days after wounding. Inflammatory cell numbers and metalloproteinase-9 levels were reduced in the propranolol-treated group compared to the control group 14 days after wounding. Cell proliferation, mast cell number, collagen deposition, blood vessel density, and nitric oxide levels were increased in the propranolol-treated group compared to the control group 14 days after wounding. Propranolol administration improves cutaneous wound healing of hyperglycemic diabetic rats by reducing the local inflammatory response and improving subsequent phases of the repair process.
Fatty acids are bioactive molecules, but their effects on cutaneous wound healing are not well understood. Our aim was to investigate the effects of supplementation with edible oils on cutaneous healing. Thirty days before wounding, rats were started on daily supplements of sunflower oil, linseed oil, fish oil, or water. Supplementation lasted until euthanasia. On day 0, an excisional wound was made on the back of each animal. Fourteen days later, the animals were euthanized, and the wound and adjacent skin were collected. Wound closure was higher in the control group compared with the other groups at days 7 and 14. Inflammatory cells were abundant in the control, linseed, and fish groups, but scarce in the sunflower group. Large numbers of myofibroblasts were observed in the control and sunflower groups. The linseed and fish groups presented a high density of dilated blood vessels. The control and sunflower groups showed a moderate density of collagen fibers; a high density of fibers was observed in the linseed and fish groups. Hydroxyproline levels were lowest in the control and sunflower groups. Supplementation with different types of edible oils delayed wound closure and affected the inflammatory infiltrate and collagen deposition.
Holoprosencephaly (HPE) is genetically heterogeneous. Variable phenotypic manifestations within families with normal and affected patients have been attributed to the number and type of HPE gene mutations. Environmental agents may also contribute to the severity as well as the requirement of multiple hits. Clinical expression is extremely variable ranging from minor facial signs to complex craniofacial anomalies such as cyclopia. Main genes involved include SHH, GLI2, PTCH1, TGIF, ZIC2, TDGF1, SIX3; however, several other candidates have been proposed. Recently it was established that the human growth arrest specific gene 1 (GAS1) is a potential locus for several human craniofacial malformations. Here, we report on four Brazilian patients with GAS1 DNA sequence change who presented variable phenotypical manifestations ranging from classic HPE to HPE-like signs. Two patients had single DNA sequence change in the GAS1 gene, while in other two, an additional mutation in the SHH gene was observed. Clinical manifestations presented by these patients suggest that GAS1 could be considered a candidate locus for one of the types of human HPE.
Administration of (low-dose) propranolol improves healing of burned rats, reducing the local inflammatory response and improving subsequent healing phases.
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