作者: ANNA CATANIA , RENÉ DELGADO , LORENA AIRAGHI , MARIAGRAZIA CUTULI , LETIZIA GAROFALO
DOI: 10.1111/J.1749-6632.1999.TB08675.X
关键词:
摘要: Until recently, inflammation was believed to arise from events taking place exclusively in the periphery. However, it is now clear that central neurogenic influences can either enhance or modulate peripheral inflammation. Therefore, should be possible improve treatment of by use antiinflammatory agents reduce host responses and inhibit proinflammatory signals nervous system (CNS). One such strategy could based on alpha-melanocyte stimulating hormone (alpha-MSH). Increases circulating TNF-alpha nitric oxide (NO), induced intraperitoneal administration endotoxin mice, were modulated injection a small concentration alpha-MSH. Inducible synthase (iNOS) activity iNOS mRNA lungs liver likewise Increase lung myeloperoxidase (MPO) significantly less mice treated with Proinflammatory greater after blockade The results suggest neural origin are triggered alpha-MSH used treat systemic In addition its influences, has inhibitory effects cells, which reduces release mediators. chemotaxis human neutrophils production TNF-alpha, neopterin, NO monocytes. research septic patients, inhibited interleukin-1 beta (IL-1 beta), interleukin-8 (IL-8) whole blood samples vitro. Combined beneficial sepsis.