The effects of apelin-13 in a mouse model of post-traumatic stress disorder.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-12-04 Epub Date: 2024-09-30 DOI:10.1097/WNR.0000000000002104
Yang Zhou, Zijun Meng, Yuqing Han, Xiaofang Yang, Jinxia Kuai, Haijun Bao
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Abstract

The objective is to investigate the effects of apelin-13 in models of post-traumatic stress disorder (PTSD). Mature male CD1 mice were subjected to the single prolonged stress method to induce PTSD-related behaviors. These behaviors were then evaluated using the elevated plus maze test, Morris water maze test, and open field test. Hippocampal neural cell death was assessed using propidium iodide labeling. The expression of hippocampal autophagy pathway-associated proteins was determined through immunoblotting analysis, and LC3 levels were also measured via quantitative real-time reverse transcription-PCR. The results demonstrate that administration of apelin-13 suppressed PTSD-induced hippocampal neural cell death and alleviated PTSD-related behaviors in mice. Additionally, PTSD led to an up-regulation of LC3 and FoxO3a, and down-regulation of P62, p-PI3K, p-Akt, and p-FoxO3a in the hippocampus. However, these changes were reversed by apelin-13 treatment. These findings support the hypothesis that apelin-13 prevents the development of PTSD-like behavior and inhibits autophagy of neuronal cells in a mouse model of PTSD. Apelin-13 may hold potential as a therapeutic agent for PTSD in clinical applications.

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apelin-13 在创伤后应激障碍小鼠模型中的作用。
目的是研究apelin-13在创伤后应激障碍(PTSD)模型中的作用。对成年雄性 CD1 小鼠采用单次长时间应激法诱导创伤后应激障碍相关行为。然后使用高架加迷宫试验、莫里斯水迷宫试验和开阔地试验对这些行为进行评估。使用碘化丙啶标记法评估海马神经细胞死亡。通过免疫印迹分析确定了海马自噬途径相关蛋白的表达,并通过实时逆转录-PCR定量检测了LC3的水平。研究结果表明,施用apelin-13能抑制创伤后应激障碍诱导的小鼠海马神经细胞死亡,并缓解创伤后应激障碍相关行为。此外,创伤后应激障碍还导致海马中 LC3 和 FoxO3a 的上调,以及 P62、p-PI3K、p-Akt 和 p-FoxO3a 的下调。然而,这些变化在apelin-13治疗后被逆转。这些发现支持了一个假设,即在创伤后应激障碍小鼠模型中,凋亡素-13可防止创伤后应激障碍样行为的发生并抑制神经元细胞的自噬。凋亡素-13有可能作为创伤后应激障碍的治疗药物应用于临床。
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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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