Amin A R, Patel R N, Thakker G D, Lowenstein C J, Attur M G, Abramson S B
Department of Rheumatology and Medicine, Hospital for Joint Diseases, New York, NY 10003, USA.
FEBS Lett. 1997 Jun 30;410(2-3):259-64. doi: 10.1016/s0014-5793(97)00605-4.
Chemically modified tetracyclines [CMT-3 (IC50 approximately 6-13 microM = approximately 2.5-5 microg/ml) and CMT-8 (IC50 approximately 26 microM = 10 microg/ml), but not CMT-1, -2 or -5], which lack anti-microbial activity, inhibited nitrite production in LPS-stimulated macrophages. Unlike competitive inhibitors of L-arginine which inhibited the specific activity of inducible nitric oxide synthase (iNOS) in cell-free extracts, CMTs exerted no such direct effect on the enzyme. CMTs could, however, be shown to inhibit both iNOS mRNA accumulation and protein expression in LPS-stimulated cells. Tetracyclines (doxycycline and CMT-3) unlike hydrocortisone had no significant effect on murine macrophages transfected with iNOS promoter (tagged to a luciferase reporter gene) in the presence of LPS. However, doxycycline and CMT-3 augmented iNOS mRNA degradation, in LPS-stimulated murine macrophages. These studies show a novel mechanism of action of tetracyclines which harbours properties to increase iNOS mRNA degradation and decrease iNOS protein expression and nitric oxide production in macrophages. This property of tetracyclines may have beneficial effects in the treatment of various diseases where excess nitric oxide has been implicated in the pathophysiology of these diseases.
化学修饰的四环素[CMT - 3(IC50约为6 - 13微摩尔=约2.5 - 5微克/毫升)和CMT - 8(IC50约为26微摩尔= 10微克/毫升),但不是CMT - 1、- 2或- 5],它们缺乏抗菌活性,可抑制脂多糖刺激的巨噬细胞中亚硝酸盐的产生。与抑制无细胞提取物中诱导型一氧化氮合酶(iNOS)比活性的L - 精氨酸竞争性抑制剂不同,CMT对该酶没有这种直接作用。然而,可以证明CMT能抑制脂多糖刺激的细胞中iNOS mRNA的积累和蛋白质表达。与氢化可的松不同,四环素(强力霉素和CMT - 3)在脂多糖存在的情况下,对转染了iNOS启动子(与荧光素酶报告基因相连)的小鼠巨噬细胞没有显著影响。然而,强力霉素和CMT - 3可增强脂多糖刺激的小鼠巨噬细胞中iNOS mRNA的降解。这些研究显示了四环素的一种新作用机制,其具有增加巨噬细胞中iNOS mRNA降解、降低iNOS蛋白表达和一氧化氮产生的特性。四环素的这一特性可能对治疗多种疾病具有有益作用,在这些疾病的病理生理学中,过量的一氧化氮被认为起了作用。