Wortmannin, a specific inhibitor of phosphatidylinositol-3-kinase, enhances LPS-induced NO production from murine peritoneal macrophages
Wortmannin, a specific inhibitor of phosphatidylinositol-3-kinase, enhances LPS-induced NO production from murine peritoneal macrophages
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DOI：
10.1006/bbrc.1997.7722
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发表时间：
1997-11-26
影响因子：
3.1
通讯作者：
Kim, HD
中科院分区：
文献类型：
--
作者：
Park, YC;Lee, CH;Kim, HD
为了阐明磷脂酰肌醇-3-激酶（PI 3 K）在巨噬细胞活化过程中的作用，我们研究了一种特异性PI 3 K抑制剂渥曼青霉素（wortmannin）对脂多糖（LPS）刺激的巨噬细胞诱导一氧化氮（NO）合成和肿瘤坏死因子-α（TNF-α）分泌的影响。Wortmannin本身对NO合成和TNF-α分泌无影响。Wortmannin以剂量依赖性方式显著增强LPS诱导的NO生成。Western blot分析表明，显着增加的iNOS蛋白表达水平在LPS刺激的巨噬细胞与渥曼青霉素治疗，相比，那些没有LPS。此外，在用渥曼青霉素处理的LPS刺激的巨噬细胞活化的起始阶段观察到TNF-α分泌的增强。这些结果表明，PI 3 K在LPS诱导的巨噬细胞活化的信号转导中起重要作用。(C)北京：科学出版社.
To elucidate the role of phosphatidylinositol-3-kinase (PI3K) during macrophage activation, we examined the effects of wortmannin, a specific inhibitor of PI3K, on the induction of nitric oxide (NO) synthesis and tumor necrosis factor-alpha (TNF-alpha) secretion from lipopolysaccharide (LPS) stimulated macrophages. Wortmannin had no effects on NO synthesis and TNF-alpha secretion by itself. Wortmannin markedly potentiated the LPS-induced NO production in a dose-dependent manner. Western blot analysis demonstrated that significantly increased levels of iNOS protein were expressed in LPS-stimulated macrophages treated with wortmannin, compared to those without LPS. Furthermore, enhancement of TNF-alpha secretion was observed in the initiation stage for activation of LPS-stimulated macrophages treated with wortmannin. These results suggest that PI3K plays an important role in transducing the signal that is involved in LPS-induced macrophage activation. (C) 1997 Academic Press.