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作 者:潘海丽 刘一丹 黄茜 杨旭娟 闫东明 刘军锋 PAN Haili;LIU Yidan;HUANG Xi;YANG Xujuan;YAN Dongming;LIU Junfeng(School of Pharmacy,Kunming Medical University,Yunnan Province,Kunming650000,China;Department of Pharmacology,Kunming Pharmaceutical Group Co.,Ltd.,Yunnan Province,Kunming650100,China)
机构地区:[1]昆明医科大学药学院,云南昆明650000 [2]昆药集团股份有限公司药理学部,云南昆明650100
出 处:《中国当代医药》2024年第34期193-198,共6页China Modern Medicine
摘 要:脑卒中是一种高致残率和高致死率的神经系统疾病,其中以缺血性脑卒中较为常见。硝化应激及其相关分子事件在缺血性脑卒中的病理过程中起重要作用。在病理状态下,由于谷氨酸受体的过度激活与一氧化氮合酶活性异常,导致细胞内产生高水平、对细胞具有毒性的活性氮。高浓度的活性氮通过S-亚硝基化、蛋白质酪氨酸硝基化破坏细胞中蛋白质的结构与功能,以及多种细胞信号传导作用导致线粒体功能障碍、DNA损伤、多聚腺苷二磷酸-核糖聚合酶激活,从而对细胞造成直接损伤;同时其通过介导炎症因子与基质金属蛋白的分泌,引发炎症和血脑屏障破坏。本研究对硝化应激及其相关分子在缺血性脑卒中造成神经细胞损伤的作用机制进行综述,寻找阻止硝化应激的靶点,以期为缺血性脑卒中治疗方案的制定提供思路和参考。Stroke is a neurological disease with a high disabling and fatal rate,among which ischemic stroke is more common.Nitrification stress and its associated molecular events play an important role in the pathological process of ischemic stroke,in which high levels of toxic reactive nitrogen are produced in cells due to the overactivation of glutamate receptors and abnormal nitric oxide synthase activity.High concentrations of reactive nitrogen destroy the structure and function of proteins in cells through S-nitrosylation and protein tyrosine nitration,as well as a variety of cell signaling effects lead to mitochondrial dysfunction,DNA damage,and poly adenosine diphosphate-ribose polymerase activation,thereby causing direct damage to cells.At the same time,it mediates the secretion of inflammatory factors and matrix metalloproteins,causing inflammation and blood-brain barrier disruption.In this study,we reviewed the mechanism of nitrification stress and its related molecules in causing nerve cell damage in ischemic stroke,and sought targets to prevent nitrification stress,in order to provide ideas and references for the formulation of treatment regimens for ischemic stroke.
关 键 词:硝化应激 过氧亚硝基阴离子 缺血性脑卒中 活性氮
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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