脓毒症线粒体损伤的氧化应激机制及靶向抗氧化剂的研究

Oxidative stress of mitochondrial injury mechanism and targeted antioxidant in sepsis

线粒体是细胞氧化的重要部位，在脓毒症时氧化应激作为炎症反应最终的结果，可引起线粒体的改变，从而可能导致器官功能损伤。在正常情况下，抗氧化防御系统通过相互作用可以对抗氧化应激，预防对线粒体的损伤。氧化应激在器官功能损伤的过程中起着重要的作用，目前已有研究发现针对线粒体的抗氧化剂靶向治疗可能是脓毒症引起的多器官功能衰竭治疗的一种新策略。该文就氧化应激在脓毒症线粒体损伤机制及靶向抗氧化剂的研究作一综述。

Mitochondria is an important part of cell oxidation, but oxidative stress in sepsis as end product of inflammation will cause changes of mitochondria, leading to organ damage. In general, antioxidant defense system fights oxidative stress through the interaction and prevents mitochondrial injury. Oxidative stress plays a important role in organ dysfunction. Studies have found that the targeted therapies for mitochondrial antioxidants may be a new strategy of multiple organ failure caused by sepsis. This review aims to summarize researches on oxidative stress of mitochondrial injury mechanism and targeted antioxidants in sepsis .