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Antioxidant pharmacological therapies for COPD

机译:慢性阻塞性肺病的抗氧化药理疗法

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摘要

Increased oxidative stress occurs in the lungs and systemically in COPD, which plays a role in many of the pathogenic mechanisms in COPD. Hence, targeting local lung and systemic oxidative stress with agents that modulate the antioxidants/redox system or boost endogenous antioxidants would be a useful therapeutic approach in COPD. Thiol antioxidants (N-acetyl-l-cysteine [NAC] and N-acystelyn, carbocysteine, erdosteine, and fudosteine) have been used to increase lung thiol content. Modulation of cigarette smoke (CS) induced oxidative stress and its consequent cellular changes have also been reported to be effected by synthetic molecules, such as spin traps (α-phenyl-N-tert- butyl nitrone), catalytic antioxidants (superoxide dismutase [ECSOD] mimetics), porphyrins, and lipid peroxidation and protein carbonylation blockers/inhibitors (edaravone and lazaroids/tirilazad). Preclinical and clinical trials have shown that these antioxidants can reduce oxidative stress, affect redox and glutathione biosynthesis genes, and proinflammatory gene expression. In this review the approaches to enhance lung antioxidants in COPD and the potential beneficial effects of antioxidant therapy on the course of the disease are discussed.
机译:氧化应激增加发生在肺部和全身性COPD中,这在COPD的许多致病机制中起作用。因此,用调节抗氧化剂/氧化还原系统或增强内源性抗氧化剂的药物靶向局部肺和全身氧化应激将是COPD中一种有用的治疗方法。硫醇抗氧化剂(N-乙酰基-1-半胱氨酸[NAC]和N-乙酰半胱氨酸,碳半胱氨酸,Erdosteine和Fudosteine)已用于增加肺硫醇含量。香烟烟雾(CS)诱导的氧化应激的调节及其随之而来的细胞变化也据报道受到合成分子的影响,例如自旋阱(α-苯基-N-叔丁基硝酮),催化抗氧化剂(超氧化物歧化酶[ECSOD ]模拟物),卟啉,脂质过氧化和蛋白质羰基化阻滞剂/抑制剂(依达拉奉和lazaroids / tirilazad)。临床前和临床试验表明,这些抗氧化剂可以减少氧化应激,影响氧化还原和谷胱甘肽的生物合成基因以及促炎基因的表达。在这篇综述中,讨论了在COPD中增强肺部抗氧化剂的方法以及抗氧化剂治疗对疾病进程的潜在有益作用。

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