Yu S M
Department of Pharmacology, Chang Gung Medical College, Kwei-San, Tao-Yuan, Taiwan.
Biochem J. 1994 Oct 1;303 ( Pt 1)(Pt 1):289-94. doi: 10.1042/bj3030289.
Formation of nitrites/nitrates caused by lipopolysaccharide (LPS) in J774.2 macrophages was inhibited by thaliporphine, an aporphine derivative isolated from the plant Neolitsea konishii K. This inhibition of nitrite synthesis in LPS-stimulated macrophages by thaliporphine was similar to that by cycloheximide, NG-methyl-L-arginine (MeArg) and dexamethasone. Thaliporphine, but not MeArg, inhibited expression of inducible NO synthase without directly affecting enzyme activity. However, thaliporphine did not inhibit nitrite production by NO synthase that had already been induced by prior exposure to LPS for which any possible further induction was inhibited by cycloheximide. In endothelial cells, nitrite formation induced by bradykinin (in the presence of 0.2 mM Ca2+) was inhibited by MeArg. However, incubation of endothelial cells with dexamethasone, cycloheximide and thaliporphine did not affect this Ca(2+)-dependent nitrite production. Thaliporphine (0.1-100 microM) dose-dependently inhibited nitrite accumulation in macrophages stimulated by interleukin-1 beta (IL-1 beta) whereas nitrite formation induced by tumour necrosis factor alpha was not inhibited. LPS-stimulated IL-1 beta synthesis in macrophages was significantly inhibited by thaliporphine, but thaliporphine had only minimal effect on LPS-stimulated IL-1 beta synthesis in endothelial cells. These results demonstrate that thaliporphine inhibits LPS induction of NO synthase expression, and that the mechanism of action of thaliporphine is via inhibition of LPS-stimulated IL-1 beta synthesis in macrophages. In anaesthetized rats subjected to LPS, pretreatment with thaliporphine partially restored the fall in mean arterial pressure and the vascular hyporeactivity to noradrenaline 3 h after LPS injection. In conclusion, thaliporphine selectively inhibited expression of inducible NO synthase, and may thus hold potential for the treatment of endotoxaemia.
从植物新木姜子中分离得到的阿朴菲衍生物去甲莲叶木碱,可抑制脂多糖(LPS)诱导J774.2巨噬细胞生成亚硝酸盐/硝酸盐。去甲莲叶木碱对LPS刺激的巨噬细胞中亚硝酸盐合成的抑制作用,与放线菌酮、NG-甲基-L-精氨酸(MeArg)和地塞米松的抑制作用相似。去甲莲叶木碱可抑制诱导型一氧化氮合酶的表达,但不直接影响酶活性,而MeArg则无此作用。然而,去甲莲叶木碱并不抑制先前暴露于LPS所诱导的一氧化氮合酶产生亚硝酸盐,放线菌酮可抑制LPS对一氧化氮合酶的任何可能的进一步诱导。在血管内皮细胞中,MeArg可抑制缓激肽(在0.2 mM Ca2+存在下)诱导的亚硝酸盐生成。然而,地塞米松、放线菌酮和去甲莲叶木碱处理血管内皮细胞,并不影响这种依赖Ca(2+)的亚硝酸盐生成。去甲莲叶木碱(0.1 - 100 microM)剂量依赖性地抑制白细胞介素-1β(IL-1β)刺激巨噬细胞中亚硝酸盐的积累,而肿瘤坏死因子α诱导的亚硝酸盐生成则未受抑制。去甲莲叶木碱可显著抑制LPS刺激巨噬细胞合成IL-1β,但对LPS刺激血管内皮细胞合成IL-1β的影响极小。这些结果表明,去甲莲叶木碱可抑制LPS诱导一氧化氮合酶的表达,其作用机制是通过抑制LPS刺激巨噬细胞合成IL-1β。在接受LPS处理的麻醉大鼠中,去甲莲叶木碱预处理可部分恢复LPS注射3小时后平均动脉压的下降以及血管对去甲肾上腺素的低反应性。总之,去甲莲叶木碱可选择性抑制诱导型一氧化氮合酶的表达,因此可能具有治疗内毒素血症的潜力。