下调NT-3和PI3K/AKT信号通路介导体内外砷诱导海马神经元凋亡

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety Pub Date : 2025-05-28 DOI:10.1016/j.ecoenv.2025.118372

Jia Cui , Ziqiao Guan , Xinbo Ma , Xinhua Shao , Kunyu Zhang , Man Lv , Meichen Zhang , Xiaona Liu , Yanhui Gao , Yanmei Yang

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引用次数: 0

摘要

砷是一种神经毒素，长期接触会导致认知障碍，而神经营养因子-3 （NT-3）对神经元的存活和发育至关重要。本研究旨在探讨NT-3对砷致认知障碍和神经元损伤的保护作用，并阐明其机制。体内和体外实验结果表明，亚砷酸钠损伤大鼠认知功能，降低神经元密度，诱导细胞凋亡，并伴有NT-3和PI3K/AKT通路下调。NT-3在HT-22细胞中的过表达可减轻砷引起的细胞凋亡，部分恢复PI3K/AKT通路活性。因此，我们的研究结果表明NT-3可能通过激活PI3K/AKT来抵消砷的神经毒性。

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Downregulated NT-3 and PI3K/AKT signaling pathway mediates arsenic-induced apoptosis in hippocampal neurons in vivo and in vitro

Arsenic is a neurotoxin associated with cognitive impairment following long-term exposure, while Neurotrophin-3 (NT-3) is essential for the survival and development of neurons. This study aims to explore the protective effects of NT-3 on arsenic-caused cognitive impairment and neuronal damage, as well as clarify the underlying mechanisms. In vivo and in vitro results indicated that sodium arsenite impaired cognitive function, reduced neuronal density, and induced apoptosis, which was accompanied by the down-regulation of NT-3 and the PI3K/AKT pathway. Overexpression of NT-3 in HT-22 cells mitigated apoptosis triggered by arsenic and partially restored PI3K/AKT pathway activity. Thus, our findings suggest that NT-3 may counteract the arsenic neurotoxicity by activating PI3K/AKT.

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来源期刊

Ecotoxicology and Environmental Safety 环境科学-毒理学

CiteScore

12.10

自引率

5.90%

发文量

1234

审稿时长

88 days

期刊介绍： Ecotoxicology and Environmental Safety is a multi-disciplinary journal that focuses on understanding the exposure and effects of environmental contamination on organisms including human health. The scope of the journal covers three main themes. The topics within these themes, indicated below, include (but are not limited to) the following: Ecotoxicology、Environmental Chemistry、Environmental Safety etc.