Pressure ulcer-induced oxidative organ injury is ameliorated by β-glucan treatment in rats

Pressure ulcers (PU) cause morphological and functional alterations in the skin and visceral organs. In this study we investigated the role of oxidative damage in PUs and the probable beneficial effect of β-glucan treatment against this damage. β-glucan is known to have immunomodulatory effects. Exp...

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Bibliographic Details
Published in:International immunopharmacology 2006-05, Vol.6 (5), p.724-732
Main Authors: Şener, Göksel, Sert, Gülten, Özer Şehirli, A., Arbak, Serap, Uslu, Bahar, Gedik, Nursal, Ayanoglu-Dulger, Gül
Format: Article
Language:English
Subjects:
Administration, Oral
Administration, Topical
Alanine Transaminase - metabolism
Animals
Antioxidants - administration & dosage
Antioxidants - pharmacology
beta-Glucans - administration & dosage
beta-Glucans - pharmacology
Biological and medical sciences
Collagen - metabolism
Decubitus ulcer
Female
Glutathione
Glutathione - metabolism
Ileum - drug effects
Ileum - metabolism
Kidney - drug effects
Kidney - metabolism
Lipid peroxidation
Lung - drug effects
Lung - metabolism
Male
Malondialdehyde - metabolism
Medical sciences
Myeloperoxidase activity
Neutrophil Infiltration - drug effects
Oxidative Stress
Peroxidase - metabolism
Pharmacology. Drug treatments
Pressure Ulcer - drug therapy
Pressure Ulcer - metabolism
Pressure Ulcer - pathology
Rats
Rats, Wistar
Reperfusion Injury
Skin - drug effects
Skin - metabolism
Skin - pathology
Stomach - drug effects
Stomach - metabolism
β-glucan
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Summary:Pressure ulcers (PU) cause morphological and functional alterations in the skin and visceral organs. In this study we investigated the role of oxidative damage in PUs and the probable beneficial effect of β-glucan treatment against this damage. β-glucan is known to have immunomodulatory effects. Experiments were carried on Wistar albino rats. PU was induced by applying magnets over steel plates that were implanted under the skin, to compress the skin and cause ischemia where removing the magnets cause reperfusion of the tissue. Within the first 12 h, rats were subjected to 5 cycles of ischemia/reperfusion (I/R), followed by 12 h ischemia. This protocol was repeated for 3 days. In treatment groups, twice a day during reperfusion periods, β-glucan was either applied locally (25 mg/kg) as an ointment on skin, or administered orally (50 mg/kg) as a gavage. At the end of the experimental periods, tissue samples (skin, liver, kidney, lung, stomach, and ileum) were taken for the measurement of malondialdehyde (MDA) – an index of lipid peroxidation – and glutathione (GSH) – a key antioxidant – levels. Neutrophil infiltration was evaluated by the measurement of tissue myeloperoxidase activity, while collagen contents were measured for the evaluation of tissue fibrosis. Skin tissues were also examined microscopically. Liver and kidney functions were assayed in serum samples. Local treatment with β-glucan inhibited the increase in MDA and MPO levels and the decrease in GSH in the skin induced by PU, but was less efficient in preventing the damage in visceral organs. However, systemic treatment prevented the damage in the visceral organs. Significant increases in creatinine, BUN, ALT, AST, LDH and collagen levels in PU group were prevented by β-glucan treatment. The light microscopic examination exhibited significant degenerative changes in dermis and epidermis in the PU group. Tissue injury was decreased especially in the locally treated group. Thus, supplementing geriatric and neurologically impaired patients with adjuvant therapy of β-glucan may have some benefits for successful therapy and improving quality of life.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2005.10.010