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新生儿缺氧缺血性脑病的氧化和抗氧化生物标志物谱:对发病机制和治疗策略的见解。

Oxidative and Antioxidative Biomarker Profiles in Neonatal Hypoxic-Ischemic Encephalopathy: Insights for Pathophysiology and Treatment Strategies.

机构信息

Department of Pediatrics, Yuzuncu Yil University, Van, Turkey.

Department of Chemistry, Yuzuncu Yil University, Van, Turkey.

出版信息

Med Sci Monit. 2024 Aug 17;30:e945045. doi: 10.12659/MSM.945045.

DOI:10.12659/MSM.945045
PMID:39152631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11337971/
Abstract

BACKGROUND Neonatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of perinatal and postnatal morbidity and mortality worldwide. Catalase (CAT) activity detection is used to determine levels of inflammation and oxidative stress. Glutathione (GSH) is the most critical non-enzymatic endogenous antioxidant. Lipid peroxidation levels marked after hypoxia can be detected based on the level of malondialdehyde (MDA). Ischemia-modified albumin (IMA) is considered a biomarker for cardiac ischemia and is known to increase in the liver, brain, and kidney in states of insufficient oxygenation. We aimed to explain the results and relations between the oxidant and antioxidants to detail oxidant-antioxidant balance and cellular mechanisms. MATERIAL AND METHODS Serum levels of IMA and MDA, as an oxidative stress marker, and CAT and GSH, as antioxidant enzymes, were measured in first blood samples of 59 neonates diagnosed with HIE, with pH <7, base excess >12, and APGAR scores. RESULTS Neonates who were ≥37 weeks of gestation and had hypoxia were included. Compared with healthy newborns (n=32), CAT was statistically significantly lower in the hypoxia group (P=0.0001), while MDA serum levels were significantly higher in neonates with hypoxia (P=0.01). There was no difference between hypoxic and healthy neonates in GSH and IMA measurements (P=0.054, P=0.19 respectively). CONCLUSIONS HIE pathophysiology involves oxidative stress and mitochondrial energy production failure. Explaining the pathways between oxidant-antioxidant balance and cell death, which explains the pathophysiology of HIE, is essential to develop treatment strategies that will minimize the effects of oxygen deprivation on other body organs, especially the brain.

摘要

背景

新生儿缺氧缺血性脑病(HIE)是全球围产期和产后发病率和死亡率的重要原因。过氧化氢酶(CAT)活性检测用于确定炎症和氧化应激水平。谷胱甘肽(GSH)是最重要的非酶内源性抗氧化剂。缺氧后丙二醛(MDA)水平升高可检测脂质过氧化水平。缺血修饰白蛋白(IMA)被认为是心肌缺血的生物标志物,已知在缺氧状态下肝脏、大脑和肾脏中会增加。我们旨在解释氧化剂和抗氧化剂之间的结果和关系,以详细说明氧化还原平衡和细胞机制。

材料和方法

在诊断为 HIE 的 59 名新生儿的第一份血样中测量了 IMA 和 MDA(作为氧化应激标志物)以及 CAT 和 GSH(作为抗氧化酶)的血清水平,这些新生儿的 pH<7、碱剩余>12 和 APGAR 评分。

结果

纳入了胎龄≥37 周且有缺氧的新生儿。与健康新生儿(n=32)相比,缺氧组的 CAT 明显降低(P=0.0001),而缺氧新生儿的 MDA 血清水平明显升高(P=0.01)。缺氧和健康新生儿的 GSH 和 IMA 测量值之间没有差异(P=0.054,P=0.19 分别)。

结论

HIE 的病理生理学涉及氧化应激和线粒体能量产生失败。解释氧化剂-抗氧化剂平衡与细胞死亡之间的途径,这解释了 HIE 的病理生理学,对于开发将最大限度减少缺氧对其他身体器官(特别是大脑)的影响的治疗策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27f/11337971/bbc44092629c/medscimonit-30-e945045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27f/11337971/0f51e48d4476/medscimonit-30-e945045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27f/11337971/bbc44092629c/medscimonit-30-e945045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27f/11337971/0f51e48d4476/medscimonit-30-e945045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27f/11337971/bbc44092629c/medscimonit-30-e945045-g002.jpg

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