title: beta-glucan protects against burn-induced oxidative organ damage in rats.
abstract: Thermal injury may lead to systemic inflammatory response, and multiple organ failure. Generation of reactive oxygen radicals and lipid peroxidation play important roles in burn-induced remote organ injury. In the present study, we investigated the putative protective effect of local or systemic beta-glucan treatment on burn-induced remote organ injury. Wistar albino rats were exposed to 90 degrees C bath for 10 s to induce thermal trauma. beta-glucan (3.75 mg/rat locally or 50 mg/kg orally) or saline was administered immediately after the trauma and were repeated twice daily in 48 h groups. Rats were decapitated either 6 or 48 h after burn injury and the skin, lung, liver, ileum and kidney tissues 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 (MPO) activity, while the tumor necrosis factor-alpha (TNF-alpha) levels were measured in serum samples. Skin tissues were also examined microscopically. Severe skin scald injury (30% of total body surface area) caused significant decreases in GSH levels of the liver and intestinal tissues (p<0.01-<0.001), while MDA levels were significantly (p<0.01-p<0.001) increased at post-burn 6 and 48 h. Both local and systemic beta-glucan treatments significantly reversed (p<0.01-p<0.001) the elevations in MDA levels, while reduced GSH levels were reversed back to control levels (p<0.01-p<0.001); and the raised MPO levels were significantly decreased (p<0.05-p<0.001). The results indicate that both systemic and local administration of beta-glucan were effective against burn-induced oxidative tissue damage in the rat. beta-glucans, besides their immunomodulatory effects, have additional antioxidant properties. Therefore, beta-glucans merit consideration as therapeutic agents in the treatment of burn injuries.
authors.affiliation: Marmara University, School of Pharmacy, Department of Pharmacology, Haydarpaşa, Istanbul 34668, Turkey.
authors.forename: Hale Z
authors.initials: HZ
authors.lastname: Toklu
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Nermina
authors.initials: N
authors.lastname: Jahovic
authors.forename: Bahar
authors.initials: B
authors.lastname: Uslu
authors.forename: Serap
authors.initials: S
authors.lastname: Arbak
authors.forename: Berrak C
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000818:Animals; D002056:Burns / Q000188:drug therapy* / Q000473:pathology*; D005260:Female; D005978:Glutathione / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D014018:Tissue Distribution; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D047071:beta-Glucans / Q000627:therapeutic use*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D047071:beta-Glucans; D008315:Malondialdehyde; D009195:Peroxidase; D005978:Glutathione