کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2542265 | 1122695 | 2006 | 14 صفحه PDF | دانلود رایگان |
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 β-glucan treatment on burn-induced remote organ injury. Wistar albino rats were exposed to 90 °C bath for 10 s to induce thermal trauma. β-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-α (TNF-α) 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 β-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 β-glucan were effective against burn-induced oxidative tissue damage in the rat. β-glucans, besides their immunomodulatory effects, have additional antioxidant properties. Therefore, β-glucans merit consideration as therapeutic agents in the treatment of burn injuries.
Journal: International Immunopharmacology - Volume 6, Issue 2, February 2006, Pages 156–169