Burns : journal of the International Society for Burn Injuries · 2025
Role of DLAT in cuproptosis and autophagy in hippocampal tissue of PTSD rats with high-voltage electrical burns.
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Ge Chenyang, Zhao Xuegang, Zhang Jing, Li Peixuan, Hao Jiawen, Lu Mengyuan, Li Congying, Ge Lili, Tu Lihong, Zhang Qingfu
Аннотация
BACKGROUND: The mechanisms behind high-voltage electrical burn (HVEB)-induced post-traumatic stress disorder (PTSD) remain unclear. Accordingly, we aimed to identify the molecular changes in hippocampal tissue following HVEB-induced PTSD.
METHODS: The GSE60303 dataset was used to identify differentially expressed cuproptosis-related genes (DE-CRGs) and to perform weighted gene co-expression network analysis. A core gene and associated genes were identified, followed by enrichment analysis. Additionally, a rat model of HVEB PTSD was established, and behavioral tests were conducted. Histological assessments and the evaluation of related protein and gene expression levels were performed on hippocampal tissue.
RESULTS: Twelve DE-CRGs were identified in the hippocampal tissue of PTSD rats, with DLAT identified as the core gene. Analysis of DLAT-associated genes revealed enrichment in the cAMP signaling pathway and autophagy. Behavioral tests confirmed that HVEB induced PTSD-like behavior in rats. DLAT expression was decreased in the hippocampal tissue of HVEB PTSD rats, accompanied by changes in the expression of cuproptosis, cAMP pathway, and autophagy-related genes.
CONCLUSION: DLAT is reduced in the hippocampal tissue of HVEB PTSD rats. The downregulation of DLAT may contribute to the development of PTSD-like behaviors in HVEB rats by promoting cuproptosis, activating the cAMP pathway, and enhancing autophagy.
METHODS: The GSE60303 dataset was used to identify differentially expressed cuproptosis-related genes (DE-CRGs) and to perform weighted gene co-expression network analysis. A core gene and associated genes were identified, followed by enrichment analysis. Additionally, a rat model of HVEB PTSD was established, and behavioral tests were conducted. Histological assessments and the evaluation of related protein and gene expression levels were performed on hippocampal tissue.
RESULTS: Twelve DE-CRGs were identified in the hippocampal tissue of PTSD rats, with DLAT identified as the core gene. Analysis of DLAT-associated genes revealed enrichment in the cAMP signaling pathway and autophagy. Behavioral tests confirmed that HVEB induced PTSD-like behavior in rats. DLAT expression was decreased in the hippocampal tissue of HVEB PTSD rats, accompanied by changes in the expression of cuproptosis, cAMP pathway, and autophagy-related genes.
CONCLUSION: DLAT is reduced in the hippocampal tissue of HVEB PTSD rats. The downregulation of DLAT may contribute to the development of PTSD-like behaviors in HVEB rats by promoting cuproptosis, activating the cAMP pathway, and enhancing autophagy.