神经保护
牛血清白蛋白
海马结构
化学
脑出血
脂质过氧化
病理
药理学
氧化应激
医学
免疫学
麻醉
内科学
蛛网膜下腔出血
作者
Xiaona Li,Li Lin,Xiaowei Li,Qian Zhu,Zhanhong Xie,Yongzhen Hu,Qing-Shan Long,Xiaobing Wei,Yi-Qi Wen,Liyang Zhang,Qi-Keng Zhang,Ying-Chao Jing,Xinhua Wei,Xuesong Li
出处
期刊:Redox biology
[Elsevier]
日期:2024-09-01
卷期号:75: 103268-103268
标识
DOI:10.1016/j.redox.2024.103268
摘要
Intracerebral hemorrhage (ICH) is a prevalent hemorrhagic cerebrovascular emergency. Alleviating neurological damage in the early stages of ICH is critical for enhancing patient prognosis and survival rate. A novel form of cell death called ferroptosis is intimately linked to hemorrhage-induced brain tissue injury. Although studies have demonstrated the significant preventive impact of bovine serum albumin-stabilized selenium nanoparticles (BSA-SeNPs) against disorders connected to the neurological system, the neuroprotective effect on the hemorrhage stroke and the mechanism remain unknown. Therefore, based on the favorable biocompatibility of BSA-SeNPs, h-ICH (hippocampus-intracerebral hemorrhage) model was constructed to perform BSA-SeNPs therapy. As expected, these BSA-SeNPs could effectively improve the cognitive deficits and ameliorate the damage of hippocampal neuron. Furthermore, BSA-SeNPs reverse the morphology of mitochondria and enhanced the mitochondrial function, evidenced by mitochondrial respiration function (OCR) and mitochondrial membrane potential (MMP). Mechanistically, BSA-SeNPs could efficiently activate the Nrf2 to enhance the expression of antioxidant GPX4 at mRNA and protein levels, and further inhibit lipid peroxidation production in erastin-induced ferroptotic damages. Taken together, this study not only sheds light on the clinical application of BSA-SeNPs, but also provides its newly theoretical support for the strategy of the intervention and treatment of neurological impairment following ICH.
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