Arbeláez-Quintero Isaac, Palacios Mauricio
Centro de Estudios Cerebrales, Facultad de Salud, Universidad del Valle, Cali, Colombia.
Stroke Res Treat. 2017;2017:9756429. doi: 10.1155/2017/9756429. Epub 2017 May 28.
Ischemic strokes are major causes of death and disability. Searching for potential therapeutic strategies to prevent and treat stroke is necessary, given the increase in overall life expectancy. Epidemiological reports indicate that metformin is an oral antidiabetic medication that can reduce the incidence of ischemic events in patients with diabetes . Its mechanism of action has not been elucidated, but metformin pleiotropic effects involve actions in addition to glycemic control. AMPK activation has been described as one of the pharmacological mechanisms that explain the action of metformin and that lead to neuroprotective effects. Most experiments done in the cerebral ischemia model, via middle cerebral artery occlusion in rodents (MCAO), had positive results favoring metformin's neuroprotective role and involve several cellular pathways like oxidative stress, endothelial nitric oxide synthase activation, activation of angiogenesis and neurogenesis, autophagia, and apoptosis. We will review the pharmacological properties of metformin and its possible mechanisms that lead to neuroprotection in cerebral ischemia.
缺血性中风是导致死亡和残疾的主要原因。鉴于总体预期寿命的增加，寻找预防和治疗中风的潜在治疗策略很有必要。流行病学报告表明，二甲双胍是一种口服抗糖尿病药物，可降低糖尿病患者缺血事件的发生率。其作用机制尚未阐明，但二甲双胍的多效性作用除血糖控制外还涉及其他作用。AMPK激活已被描述为解释二甲双胍作用并导致神经保护作用的药理机制之一。在啮齿动物大脑中动脉闭塞（MCAO）的脑缺血模型中进行的大多数实验都取得了积极结果，支持二甲双胍的神经保护作用，并且涉及多种细胞途径，如氧化应激、内皮型一氧化氮合酶激活、血管生成和神经发生激活、自噬和凋亡。我们将综述二甲双胍的药理特性及其在脑缺血中导致神经保护的可能机制。
