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

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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Publication Details

Journal
Neuroreport
Published
2024-09-30
DOI
https://doi.org/10.1097/wnr.0000000000002104
Primary Topic
Apelin-related biomedical research
Type
article
Field-Weighted Citation Impact
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article

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

Jinxia Kuai, Zijun Meng, Yang Zhou, Xiaofang Yang et al.
Neuroreport
Apelin-related biomedical research
article

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

Jinxia Kuai, Zijun Meng, Yang Zhou, Xiaofang Yang, Yuqing Han, Haijun Bao
article en

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.

NeuroreportVol. 35(17)
Shanxi Medical University (CN), Xuzhou Medical College (CN), Shanxi Fenyang Hospital (CN)
Good health and well-being
Openalex Percentile: Top 82%
Apelin-related biomedical research
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