Abstract

Minor injuries in healthy people usually heal well, but larger wounds or the presence of various physiological (age) or pathological conditions (metabolic syndrome, obesity, diabetes, and cancer) can impede this process. The aim of our work was to determine the factors that may influence the duration of healing (growth factors and hypoxia-induced factor 1α) in the wound bed of rats with metabolic syndrome. The experiments were conducted on 80 white non-linear laboratory rats, aged 4-5 months, which were divided after birth into 2 groups of 40 animals each (20 males and 20 females). Group I rats were subcutaneously injected with saline at a dose of 8 μg/ ml on days 2, 4, 6, 8, and 10 after birth. Group II rats were administered a sodium glutamate solution at a dose of 4.0 mg/ kg at the same time. At the age of 4 months, animals of both subgroups were modeled with incised wounds . The control animals were rats in each of the groups in which wounds were not modeled. The material for biochemical studies was the skin in the areas of the former wound bed. Rats in the control group had their skin excised at the same sites as those in the experimental groups. The skin was homogenized and the content of growth factors of endothelial and nerve cells (VEGF, NGF, respectively) and hypoxia-inducible factor (HIF-1α) was determined by immuno-enzymatic method. In unoperated male rats with metabolic syndrome, the skin content of VEGF, NGF, and HIF-1a increased compared to control animals without the syndrome. In unoperated females with metabolic syndrome, VEGF levels decreased with a simultaneous increase in NGF and HIF-1α. In the wound bed of animals with metabolic syndrome, after the closure of the wound surface, the content of VEGF and HIF-1α increased, and the content of NGF remained unchanged compared with the values in unoperated rats. The results obtained indicate the involvement of growth factors VEGF and NGF and HIF-1α in prolonging the duration of healing of incised wounds in rats with metabolic syndrome. At the same time, these growth factors and HIF-1α may be involved in the mechanisms of development of some postoperative complications.

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