AI Summary & Key Takeaways
AI InsightReactive oxygen metabolite production was measured by chemiluminescence (CL) technique using luminol or lucigenin probes.Results: Lucigenin CL value of cells obtained from burn animals was significantly higher than those obtained from the sham group. α-MSH caused significant reductions in high lucigenin CL values and this effect was partly inhibited by sodium nitroprusside.Conclusion: Our results suggest that α-MSH is effective in preventing oxidant production by neutrophils activated by burn trauma, at least in part, by a mechanism involving nitric oxide.
📌 3 Key Takeaways
Abstract
Objective: Previous findings related to the anti-inflammatory effects of α-melanocyte stimulating hormone (α-MSH) indicate that the peptide might inhibit inflammation by antagonizing the effects of local cytokines or by inhibiting neutrophil functions. In addition, it is a potent inhibitor of the induction of the inducible nitric oxide synthase (iNOS) in cultured macrophages and of nitric oxide (NO) production in a sepsis model. This study was designed to investigate whether α-MSH affects reactive oxygen metabolite production by rat peritoneal neutrophils following burn injury and whether NO is involved in this effect.Methods: The neutrophils were removed from the peritoneum of the rats 6 h after burn or sham trauma. Cells (2 X 106 /ml) were treated with the increasing concentrations of α-MSH (10–12 M, 10–10 M, 10–8 M or 10–6 M). Nitric oxide donor, sodium nitroprusside ranging from (10–10 - 10–4 M) was added to the cells in the presence of α-MSH. Reactive oxygen metabolite production was measured by chemiluminescence (CL) technique using luminol or lucigenin probes.Results: Lucigenin CL value of cells obtained from burn animals was significantly higher than those obtained from the sham group. α-MSH caused significant reductions in high lucigenin CL values and this effect was partly inhibited by sodium nitroprusside.Conclusion: Our results suggest that α-MSH is effective in preventing oxidant production by neutrophils activated by burn trauma, at least in part, by a mechanism involving nitric oxide.