Author(s): Eski M, Deveci M, Celikz B, Nisanci M, Tregn M
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Abstract It is suggested that burn toxin known as lipid protein complex (LPC) stimulates phagocytic cells that cause the release of a variety of inflammatory mediators which induce the activation of leukocytes. It is reported that cerium nitrate (CN) might fix LPC in eschar tissue and prevent LPC from entering the circulation. In this study, we tested the hypothesis that prevention or modulation of LPC initiated cell activation by fixing LPC in eschar tissue with CN treatment, would reduce the number of activated leukocytes, which is an important indicator of inflammation, in rat cremaster muscle flap model. Twenty-eight animals were studied in four groups--group I (control), only cremaster muscle flap was dissected; group II (burn injury), burn injury was performed and flap was dissected; group III (saline); and group IV (CN), following burn injury rats treated with saline and CN, respectively, and than flaps were dissected. Blood vessels were observed in vivo under an intravital microscopy system and the number of rolling, sticking, and transmigrating leukocytes were measured in each group. Burn injury significantly increased the number of activated leukocytes (P<0.001). We observed that CN treatment significantly reduced the number of activated leukocytes following burn injury (P<0.001). In conclusion, we demonstrated that CN treatment significantly decreased the activation of leukocytes, which plays an important role in systemic inflammation. Decreased leukocyte activation is interpreted as prevention or modulation of systemic inflammatory response following burn injury.
This article was published in Burns
and referenced in Journal of Gastrointestinal & Digestive System