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 P-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. (c) 2005 Elsevier B.V. All rights reserved.