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一氧化氮在炎症性疾病中的作用。

Role of nitric oxide in inflammatory diseases.

作者信息

Sharma J N, Al-Omran A, Parvathy S S

机构信息

Department of Applied Therapeutics, Faculty of Pharmacy, Kuwait University, Health Sciences Centre, P.O. Box 24923, Safat, 13110, Kuwait.

出版信息

Inflammopharmacology. 2007 Dec;15(6):252-9. doi: 10.1007/s10787-007-0013-x.

Abstract

Nitric oxide (NO) is a signaling molecule that plays a key role in the pathogenesis of inflammation. It gives an anti-inflammatory effect under normal physiological conditions. On the other hand, NO is considered as a pro-inflammatory mediator that induces inflammation due to over production in abnormal situations. NO is synthesized and released into the endothelial cells by the help of NOSs that convert arginine into citrulline producing NO in the process. Oxygen and NADPH are necessary co-factors in such conversion. NO is believed to induce vasodilatation in cardiovascular system and furthermore, it involves in immune responses by cytokine-activated macrophages, which release NO in high concentrations. In addition, NO is a potent neurotransmitter at the neuron synapses and contributes to the regulation of apoptosis. NO is involved in the pathogenesis of inflammatory disorders of the joint, gut and lungs. Therefore, NO inhibitors represent important therapeutic advance in the management of inflammatory diseases. Selective NO biosynthesis inhibitors and synthetic arginine analogues are proved to be used for the treatment of NO-induced inflammation. Finally, the undesired effects of NO are due to its impaired production, including in short: vasoconstriction, inflammation and tissue damage.

摘要

一氧化氮(NO)是一种信号分子,在炎症发病机制中起关键作用。在正常生理条件下,它具有抗炎作用。另一方面,在异常情况下,由于NO产生过多,它被认为是一种促炎介质,可诱导炎症。NO是在内皮细胞中由一氧化氮合酶(NOSs)的帮助下合成并释放的,在这个过程中,NOSs将精氨酸转化为瓜氨酸并产生NO。氧气和NADPH是这种转化过程中必需的辅助因子。据信,NO在心血管系统中可诱导血管舒张,此外,它还参与细胞因子激活的巨噬细胞的免疫反应,巨噬细胞会释放高浓度的NO。此外,NO是神经元突触处一种有效的神经递质,有助于调节细胞凋亡。NO参与关节、肠道和肺部炎症性疾病的发病机制。因此,NO抑制剂在炎症性疾病的治疗中代表了重要的治疗进展。选择性NO生物合成抑制剂和合成精氨酸类似物已被证明可用于治疗NO诱导的炎症。最后,NO的不良作用是由于其产生受损,简而言之,包括血管收缩、炎症和组织损伤。

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