二甲双胍对脓毒症致器官衰竭保护作用的研究进展

Fatima Ismail Hassan, T. Didari, Fazlullah Khan, K. Niaz, M. Mojtahedzadeh, M. Abdollahi
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引用次数: 40

摘要

尽管在脓毒症管理方面取得了进展,但它仍然是重症监护病房(ICU)关注的主要问题。从新的角度来看,二甲双胍的积极作用,如抗氧化和抗炎特性,被认为是治疗脓毒症患者的潜在有益特性。本文综述了二甲双胍在脓毒症引起的器官衰竭中的潜在改善作用。信息检索自PubMed、Scopus、Embase和Google Scholar。多器官损伤、氧化应激、炎症细胞因子刺激和循环改变是败血症的标志。二甲双胍通过激活单磷酸腺苷活化蛋白激酶(AMPK)发挥其作用。它通过抑制活性氧(ROS)和促炎细胞因子的产生,阻止炎症相关转录因子的激活,减少中性粒细胞的积累/浸润,维持线粒体膜电位,改善败血症诱导的器官衰竭。研究报告了二甲双胍治疗剂量的安全性,没有证据表明在脓毒症患者中发生乳酸性酸中毒。
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A Review on The Protective Effects of Metformin in Sepsis-Induced Organ Failure
Despite advances in sepsis management, it remains a major intensive-care-unit (ICU) concern. From new prospective, positive effects of metformin, such as anti-oxidant and anti-inflammatory properties are considered potentially beneficial properties for management of septic patients. This article reviewed the potential ameliorative effects of metformin in sepsis-induced organ failure. Information were retrieved from PubMed, Scopus, Embase, and Google Scholar. Multi-organ damage, oxidative stress, inflammatory cytokine stimulation, and altered circulation are hallmarks of sepsis. Metformin exerts its effect via adenosine monophosphate-activated protein kinase (AMPK) activation. It improves sepsis-induced organ failure by inhibiting the production of reactive oxygen species (ROS) and pro-inflammatory cytokines, preventing the activation of transcription factors related to inflammation, decreasing neutrophil accumulation/infiltration, and also maintaining mitochondrial membrane potential. Studies reported the safety of metformin therapeutic doses, with no evidence of lactic acidosis, in septic patients.
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