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Regulation of oxidative stress by Nrf2 in the pathophysiology of infectious diseases

机译:Nrf2在传染病病理生理中对氧化应激的调节

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摘要

The innate immune system, including phagocytic cells, is the first line of defense against pathogens. During infection by microorganisms such as viruses, bacteria, or parasites, phagocytic cells produce an excess of oxidants, a crucial process for the clearance of pathogens. This increase in oxidants creates an imbalance between oxidants and endogenous antioxidants. Left unchecked, this acute or chronic oxidative stress can lead to apoptotic cell-death and oxidative stress-induced diseases including neurodegenerative and cardiovascular disorders, premature aging, secondary infections, and cancer. The activation of nuclear factor E2-related factor 2 (Nrf2) is an efficient antioxidant defensive mechanism used by host cells to counteract oxidative stress. The transcription factor Nrf2 has been identified as the master regulator of several hundred of genes involved in the antioxidant defense response. The review objectives were to collect recent findings on the contribution of oxidative stress to complications of infection, and to highlight the beneficial impact of antioxidants in reducing inflammation and oxidant-related tissue damage. Furthermore, a direct relationship between infection and decline in Nrf2 activity has been demonstrated. Thus, an interesting therapeutic approach in disease prevention and treatment of stress-related diseases may consist in optimizing antibiotic or antiviral therapy with a combination of Nrf2 inducer treatment.
机译:包括吞噬细胞在内的先天免疫系统是抵御病原体的第一道防线。在被病毒,细菌或寄生虫等微生物感染期间,吞噬细胞会产生过量的氧化剂,这是清除病原体的关键过程。氧化剂的这种增加在氧化剂和内源性抗氧化剂之间造成了不平衡。如果不加以控制,这种急性或慢性氧化应激可导致凋亡性细胞死亡和氧化应激诱导的疾病,包括神经变性和心血管疾病,过早衰老,继发感染和癌症。核因子E2相关因子2(Nrf2)的激活是宿主细胞用来抵消氧化应激的一种有效的抗氧化剂防御机制。转录因子Nrf2已被确定为参与抗氧化防御反应的数百个基因的主要调控因子。审查的目的是收集关于氧化应激对感染并发症的贡献的最新发现,并强调抗氧化剂在减少炎症和与氧化剂相关的组织损伤中的有益作用。此外,已证明感染与Nrf2活性下降之间存在直接关系。因此,在疾病预防和与压力有关的疾病的治疗中,有趣的治疗方法可能在于结合Nrf2诱导剂治疗优化抗生素或抗病毒治疗。

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