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垂体腺苷酸环化酶激活多肽:氧化应激中的一种有效治疗剂。

Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress.

作者信息

Sadanandan Nadia, Cozene Blaise, Park You Jeong, Farooq Jeffrey, Kingsbury Chase, Wang Zhen-Jie, Moscatello Alexa, Saft Madeline, Cho Justin, Gonzales-Portillo Bella, Borlongan Cesar V

机构信息

Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.

出版信息

Antioxidants (Basel). 2021 Feb 26;10(3):354. doi: 10.3390/antiox10030354.

DOI:10.3390/antiox10030354
PMID:33653014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7996859/
Abstract

Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body's endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. The overproduction of ROS compromises the functional and structural integrity of brain tissue. Therefore, it is essential to investigate the mechanisms involved in oxidative stress to help obtain adequate treatment options for stroke. Here, we focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.

摘要

中风是一种危及生命的疾病,其特征是在最初脑部血流中断后发生继发性细胞死亡过程。内源性修复机制无法充分支持中风患者的功能恢复,且可用的治疗选择不足,令人担忧。中风中氧化应激背后的病理因其对大脑的有害影响而备受关注。缺血性中风引起的氧化应激超过了身体内源性抗氧化系统的中和能力,导致活性氧(ROS)和活性氮(RNS)过度产生,最终导致细胞死亡。ROS的过度产生损害了脑组织的功能和结构完整性。因此,研究氧化应激所涉及的机制对于帮助获得中风的适当治疗选择至关重要。在此,我们关注最新的临床前研究,这些研究详细阐述了导致许多中枢神经系统(CNS)疾病的继发性细胞死亡过程背后的机制,以及与垂体腺苷酸环化酶激活多肽(PACAPs)的神经保护分子机制如何使这些分子成为中风治疗的理想候选药物相关的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6795/7996859/166ef28438d1/antioxidants-10-00354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6795/7996859/166ef28438d1/antioxidants-10-00354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6795/7996859/166ef28438d1/antioxidants-10-00354-g001.jpg

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