PROSTANOIDS INHIBIT KUPFFER CELL NITRIC-OXIDE SYNTHESIS

被引：22

作者：

HARBRECHT, BG

MCCLURE, EA

SIMMONS, RL

BILLIAR, TR

机构：

[1] Department of Surgery, University of Pittsburgh, Pittsburgh

来源：

JOURNAL OF SURGICAL RESEARCH | 1995年 / 58卷 / 06期

关键词：

D O I：

10.1006/jsre.1995.1098

中图分类号：

R61 [外科手术学];

学科分类号：

摘要：

Kupffer cells are the largest population of fixed tissue macrophages in the body and produce a number of mediators that are involved in host defense. These mediators include cytokines such as tumor necrosis factor-alpha and interleukin-1, prostaglandins, oxygen radicals, and nitric oxide. Prostaglandins are produced by adjacent endothelial cells in addition to Kupffer cells and regulate a number of cellular functions in a wide array of cells, but their role in nitric oxide synthesis is controversial. We studied the role of prostaglandins in regulating lipopolysaccharide (LPS)-induced nitric oxide synthesis in cultured rat Kupffer cells. Prostaglandin E(2) (PGE(2)) inhibited Kupffer cell nitric oxide synthesis in a dose-dependent fashion in both 24- and 48-hr cultures. The effect of PGE(2) persisted at low and high LPS concentrations. Prostaglandin analogues as well as other prostanoids also inhibited Kupffer cell nitric oxide synthesis. These data show that exogenous prostaglandins suppress Kupffer cell nitric oxide synthesis and may represent an important endogenous regulator of nitric oxide production. (C) 1995 Academic Press, Inc.

引用

页码：625 / 629

页数：5

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