Suppr超能文献

抑郁症的新药物靶点:炎症、细胞介导的免疫、氧化和硝化应激、线粒体、抗氧化剂和神经进展途径。以及新的药物候选物——Nrf2 激活剂和 GSK-3 抑制剂。

New drug targets in depression: inflammatory, cell-mediated immune, oxidative and nitrosative stress, mitochondrial, antioxidant, and neuroprogressive pathways. And new drug candidates--Nrf2 activators and GSK-3 inhibitors.

机构信息

Maes Clinics@TRIA, 998 Rimklongsamsen Road, Bangkok 10310, Thailand.

出版信息

Inflammopharmacology. 2012 Jun;20(3):127-50. doi: 10.1007/s10787-011-0111-7. Epub 2012 Jan 24.

Abstract

This paper reviews new drug targets in the treatment of depression and new drug candidates to treat depression. Depression is characterized by aberrations in six intertwined pathways: (1) inflammatory pathways as indicated by increased levels of proinflammatory cytokines, e.g. interleukin-1 (IL-1), IL-6, and tumour necrosis factor α. (2) Activation of cell-mediated immune pathways as indicated by an increased production of interferon γ and neopterin. (3) Increased reactive oxygen and nitrogen species and damage by oxidative and nitrosative stress (O&NS), including lipid peroxidation, damage to DNA, proteins and mitochondria. (4) Lowered levels of key antioxidants, such as coenzyme Q10, zinc, vitamin E, glutathione, and glutathione peroxidase. (5) Damage to mitochondria and mitochondrial DNA and reduced activity of respiratory chain enzymes and adenosine triphosphate production. (6) Neuroprogression, which is the progressive process of neurodegeneration, apoptosis, and reduced neurogenesis and neuronal plasticity, phenomena that are probably caused by inflammation and O&NS. Antidepressants tend to normalize the above six pathways. Targeting these pathways has the potential to yield antidepressant effects, e.g. using cytokine antagonists, minocycline, Cox-2 inhibitors, statins, acetylsalicylic acid, ketamine, ω3 poly-unsaturated fatty acids, antioxidants, and neurotrophic factors. These six pathways offer new, pathophysiologically guided drug targets suggesting that novel therapies could be developed that target these six pathways simultaneously. Both nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activators and glycogen synthase kinase-3 (GSK-3) inhibitors target the six above-mentioned pathways. GSK-3 inhibitors have antidepressant effects in animal models of depression. Nrf2 activators and GSK-3 inhibitors have the potential to be advanced to phase-2 clinical trials to examine whether they augment the efficacy of antidepressants or are useful as monotherapy.

摘要

这篇论文综述了治疗抑郁症的新药物靶点和新候选药物。抑郁症的特征是六条相互交织的途径发生异常:(1)炎症途径,表现为促炎细胞因子水平升高,例如白细胞介素-1(IL-1)、IL-6 和肿瘤坏死因子 α。(2)细胞介导的免疫途径激活,表现为干扰素 γ 和新蝶呤的产生增加。(3)活性氧和氮物种增加,氧化和硝化应激(O&NS)造成损害,包括脂质过氧化、DNA、蛋白质和线粒体损伤。(4)关键抗氧化剂水平降低,如辅酶 Q10、锌、维生素 E、谷胱甘肽和谷胱甘肽过氧化物酶。(5)线粒体和线粒体 DNA 损伤,呼吸链酶活性降低,三磷酸腺苷生成减少。(6)神经进展,即神经退行性变、细胞凋亡以及神经发生和神经元可塑性降低的进行性过程,这些现象可能是由炎症和 O&NS 引起的。抗抑郁药往往使上述六条途径正常化。针对这些途径有可能产生抗抑郁作用,例如使用细胞因子拮抗剂、米诺环素、COX-2 抑制剂、他汀类药物、乙酰水杨酸、氯胺酮、ω3 多不饱和脂肪酸、抗氧化剂和神经营养因子。这六条途径提供了新的、基于病理生理学的药物靶点,表明可以开发同时针对这六条途径的新型治疗方法。核因子(红细胞衍生 2)样 2(Nrf2)激活剂和糖原合成酶激酶-3(GSK-3)抑制剂都靶向上述六条途径。GSK-3 抑制剂在抑郁症动物模型中具有抗抑郁作用。Nrf2 激活剂和 GSK-3 抑制剂有可能进入 2 期临床试验,以检验它们是否增强抗抑郁药的疗效,或者是否可作为单一疗法使用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验