Nω-nitro-L-arginine methyl ester inhibits inflammatory liver injury induced by interleukin-2

被引:0
作者
Lentsch, AB [1 ]
Edwards, MJ
Sims, DE
Miller, FN
机构
[1] Univ Louisville, Dept Surg, Louisville, KY 40292 USA
[2] Univ Louisville, Dept Physiol & Biophys, Louisville, KY 40292 USA
[3] Univ Louisville, Ctr Appl Microcirculatory Res, Louisville, KY 40292 USA
[4] Univ Prince Edward Isl, Atlantic Vet Coll, Dept Anat & Physiol, Charlottetown, PE C1A 4P3, Canada
关键词
cytokines; nitric oxide; inflammation; hepatocellular injury;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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-8-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 leukocytes and platelet adhesion. Administration of IL-2 increased leukocyte and platelet adhesion in postsinusoidal 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 ma?; play a central role in IL-2-induced inflammatory liver injury.
引用
收藏
页码:22 / 30
页数:9
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