N omega-nitro-L-arginine methyl ester inhibits inflammatory liver injury induced by interleukin-2
| Autor: | A B, Lentsch, M J, Edwards, D E, Sims, F N, Miller |
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| Rok vydání: | 1998 |
| Předmět: |
Male
Platelet Count Liver Diseases Alanine Transaminase Blood Pressure Thrombosis Nitric Oxide Mice Inbred C57BL Mice NG-Nitroarginine Methyl Ester Platelet Adhesiveness Liver Cell Adhesion Animals Edema Interleukin-2 Aspartate Aminotransferases Endothelium Vascular Chemical and Drug Induced Liver Injury Enzyme Inhibitors Nitric Oxide Synthase |
| Zdroj: | Journal of leukocyte biology. 63(1) |
| ISSN: | 0741-5400 |
| Popis: | Administration of interleukin-2 (IL-2) for treatment of metastatic disease often results in inflammatory liver injury. Previous studies have implicated increased leukocyte and platelet adhesion and enhanced nitric oxide production as causative factors in the development of IL-2-induced hepatic injury. This study investigated the capacity of N omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthesis inhibitor, to limit IL-2-induced hepatic edema and hepatocellular damage in mice. Using hepatic intravital microscopy, we also examined the effects of L-NAME on IL-2-induced increases in leukocyte and platelet adhesion. Administration of IL-2 increased leukocyte and platelet adhesion in post-sinusoidal venules and decreased hepatic perfusion. Cotreatment with L-NAME had no effect on leukocyte adhesion but increased platelet-endothelial adhesion and microvascular thrombosis. Chronic IL-2 treatment induced hepatic edema and hepatocellular injury. However, coadministration of L-NAME attenuated IL-2-induced edema and completely inhibited hepatocellular damage. These findings suggest that nitric oxide may play a central role in IL-2-induced inflammatory liver injury. |
| Databáze: | OpenAIRE |
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