氮饱压在潜在病理生理学中的意义及对具有排泄和抗氧化能力的非传染性疾病的药理学治疗

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摘要

慢性应激(OS)可以降解一系列物质和细胞结构,损害器官和系统的性能。内源性和外源性途径有助于OS在体内的积累。越来越多的证据表明,OS在各种需要持续药物治疗的慢性疾病的生理病理中起作用。长期治疗可能影响全身性OS。在本文中,我们探讨了OS在几种慢性疾病的病理生理中的作用,它们的药物治疗的促或抗氧化作用,以及潜在的辅助抗氧化替代品。高血压、动脉硬化和糖尿病会增加患心血管疾病的风险。降压、降脂和降糖药物有助于降低风险,同时也提供抗氧化的好处。在类风湿性关节炎等自身免疫性系统性炎症疾病中,甲氨蝶呤治疗具有促进OS合成和引起线粒体功能障碍的双重作用。然而,它也可能间接有助于减少炎症引起的系统性OS。用于治疗神经退行性疾病的药物已被证明可以抑制参与产生和平衡活性氧(ROS)的系统。另一方面,针对癌症或人类免疫缺陷病毒感染的免疫抑制治疗会增强ROS的产生,在缺乏充分记录的外源性抗氧化剂递送的情况下,导致一些器官和系统的严重氧化损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Significance of Nitrosative Pressure in Underlying Pathophysiology and The Pharmacologic Therapy of Non-Communicable Disease with Fessional and Antioxidant Potential
Chronic stress (OS) can degrade a range of substances and cellular structures, impairing organ and system performance. Endogenous and external pathways contribute to the accumulation of OS in the body. There is mounting evidence that OS has a role in the physiopathology of various chronic disorders that require continuous pharmaceutical treatment. Prolonged therapy may affect systemic OS. We explore the role of OS in the pathophysiology of several chronic diseases, the pro- or antioxidant effects of their pharmaceutical therapies, and potential adjuvant antioxidant alternatives in this review. High blood pressure, arteriosclerosis, and diabetes mellitus raise the risk of developing cardiovascular disease. Antihypertensive, lipid-lowering, and hypoglycemic medications contribute to risk reduction while also providing an antioxidant benefit. In autoimmune systemic inflammatory illnesses such as rheumatoid arthritis, methotrexate treatment has a dual effect of boosting OS synthesis and causing mitochondrial malfunction. However, it may also contribute indirectly to reducing systemic OS caused by inflammation. Medications used to treat neurodegenerative illnesses have been shown to inhibit systems involved in producing and balancing reactive oxygen species (ROS). On the other hand, immunosuppressive treatments for cancer or human immunodeficiency virus infection enhance ROS generation, resulting in severe oxidative damage in several organs and systems in the absence of welldocumented exogenous antioxidant delivery.
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