Publication: Nesfatin-1 improves oxidative skin injury in normoglycemic or hyperglycemic rats
No Thumbnail Available
Date
2016
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
ELSEVIER SCIENCE INC
Abstract
Hyperglycemia is one of the major causes of suppressed angiogenesis and impaired wound healing leading to chronic wounds. Nesfatin-1 a novel peptide was reported to have antioxidant and anti-apoptotic properties. This study is aimed to investigate the potential healing-promoting effects of nesfatin-1 in non diabetic or diabetic rats with surgical wounds. In male Sprague-Dawley rats, hyperglycemia was induced by intraperitoneal (ip) injection of streptozotocin (55 mg/kg). Under anesthesia, dorsum skin tissues of normoglycemic (n = 16) and hyperglycemic rats were excised (2 x 2 cm, full-thickness), while control rats (n = 16) had neither hyperglycemia nor wounds. Half of the rats in each group were treated ip with saline, while the others were treated with nesfatin-1 (2 g/kg/day) for 3 days until they were decapitated. Plasma interleukin-1-beta (IL-1 beta), transforming growth factor-beta (TGF-beta-1), IL-6 levels, and dermal tissue malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) and caspase-3 activity were measured. For histological examination, paraffin sections were stained with hematoxylin-eosin or Masson's trichrome and immunohistochemistry for vascular endothelial growth factor (VEGF) was applied. ANOVA and Student's t-tests were used for statistical analysis. Compared to control rats, skin MPO activity, MDA and caspase-3 levels were increased similarly in saline-treated normo- and hyperglycemic rats. Nesfatin-1 depressed MDA, caspase-3, MPO activity and IL-1 beta with concomitant elevations in dermal GSH and plasma TGF-beta-1 levels. Histopathological examination revealed regeneration of epidermis, regular arrangement of collagen fibers in the dermis and a decrease in VEGF immunoreactivity in the epidermal keratinocytes of nesfatin-1-treated groups. Nesfatin-1 improved surgical wound healing in both normo- and hyperglycemic rats via the suppression of neutrophil recruitment, apoptosis and VEGF activation. (C) 2016 Elsevier Inc. All rights reserved.
Description
Keywords
Nesfatin-1, Vascular endothelial growth factor (VEGF), Hyperglycaemia, Surgical wound, Neutrophil infiltration, Oxidative injury, ENDOTHELIAL GROWTH-FACTOR, FACTOR EXPRESSION, ANTIOXIDANT, INSULIN, BETA, IMMUNOREACTIVITY, GLUTATHIONE, STRESS, ULCERS, DAMAGE