Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression

ABSTRACT Background Depression is a global health concern characterized by high incidence, disability, and disease burden. Neuroimmunity, through the secretion of inflammatory mediators and mediation of neuroinflammation, plays a significant role in depression's pathogenesis. However, the under...

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Main Authors: Wen‐Wen Li, Rui Xiao, Xue‐Yi Chen, Jun‐Cai Pu, Jian‐Jun Chen, Hai‐Yang Wang, Lan‐Xiang Liu, Dan Li, Yang‐Dong Zhang, Wen‐Xia Li, Peng Xie
Format: Article
Language:English
Published: Wiley 2025-05-01
Series:Brain and Behavior
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Online Access:https://doi.org/10.1002/brb3.70549
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author Wen‐Wen Li
Rui Xiao
Xue‐Yi Chen
Jun‐Cai Pu
Jian‐Jun Chen
Hai‐Yang Wang
Lan‐Xiang Liu
Dan Li
Yang‐Dong Zhang
Wen‐Xia Li
Peng Xie
author_facet Wen‐Wen Li
Rui Xiao
Xue‐Yi Chen
Jun‐Cai Pu
Jian‐Jun Chen
Hai‐Yang Wang
Lan‐Xiang Liu
Dan Li
Yang‐Dong Zhang
Wen‐Xia Li
Peng Xie
author_sort Wen‐Wen Li
collection DOAJ
description ABSTRACT Background Depression is a global health concern characterized by high incidence, disability, and disease burden. Neuroimmunity, through the secretion of inflammatory mediators and mediation of neuroinflammation, plays a significant role in depression's pathogenesis. However, the underlying molecular mechanisms remain poorly understood. Methods In this pioneering study, we employed a comprehensive multi‐omics approach, integrating 2‐DE proteomics, liquid chromatography mass spectrometry‐based metabolomics, and real‐time polymerase chain reaction (PCR) array, to investigate the hippocampal molecular profiles of lipopolysaccharide (LPS)‐induced immune inflammation‐related depression. This innovative approach aimed to explore the potential pathogenesis of depression by systematically integrating data across multiple molecular layers. Results Compared to the control group, we identified 81 differential proteins, 44 differential metabolites, and 4 differential mRNAs in LPS‐treated mice. Integrated analysis of these multidimensional data revealed that purine metabolism and glutamate metabolism are the most significantly altered molecular pathways in LPS‐induced depression. Additionally, we constructed the corresponding compound‐reaction‐enzyme‐gene regulatory network. Conclusion This study suggests that purine metabolism and glutamate metabolism may be the underlying mechanisms by which neuroinflammation regulates depression‐like behaviors. Our findings confirm the important role of immune inflammation in depression and provide a new clue for the diagnosis and treatment of this disorder. Notably, the multi‐omics approach employed in this study represents a pioneering effort in the field, providing unprecedented insights into the molecular mechanisms underlying depression.
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spelling doaj-art-d5a387aa1da440c29bced74b4cd822312025-08-20T02:29:19ZengWileyBrain and Behavior2162-32792025-05-01155n/an/a10.1002/brb3.70549Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of DepressionWen‐Wen Li0Rui Xiao1Xue‐Yi Chen2Jun‐Cai Pu3Jian‐Jun Chen4Hai‐Yang Wang5Lan‐Xiang Liu6Dan Li7Yang‐Dong Zhang8Wen‐Xia Li9Peng Xie10Faculty of Basic Medicine, Department of Pathology Chongqing Medical University Chongqing ChinaFaculty of Basic Medicine, Department of Pathology Chongqing Medical University Chongqing ChinaFaculty of Basic Medicine, Department of Pathology Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaFaculty of Basic Medicine, Department of Pathology Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases The First Affiliated Hospital of Chongqing Medical University Chongqing ChinaABSTRACT Background Depression is a global health concern characterized by high incidence, disability, and disease burden. Neuroimmunity, through the secretion of inflammatory mediators and mediation of neuroinflammation, plays a significant role in depression's pathogenesis. However, the underlying molecular mechanisms remain poorly understood. Methods In this pioneering study, we employed a comprehensive multi‐omics approach, integrating 2‐DE proteomics, liquid chromatography mass spectrometry‐based metabolomics, and real‐time polymerase chain reaction (PCR) array, to investigate the hippocampal molecular profiles of lipopolysaccharide (LPS)‐induced immune inflammation‐related depression. This innovative approach aimed to explore the potential pathogenesis of depression by systematically integrating data across multiple molecular layers. Results Compared to the control group, we identified 81 differential proteins, 44 differential metabolites, and 4 differential mRNAs in LPS‐treated mice. Integrated analysis of these multidimensional data revealed that purine metabolism and glutamate metabolism are the most significantly altered molecular pathways in LPS‐induced depression. Additionally, we constructed the corresponding compound‐reaction‐enzyme‐gene regulatory network. Conclusion This study suggests that purine metabolism and glutamate metabolism may be the underlying mechanisms by which neuroinflammation regulates depression‐like behaviors. Our findings confirm the important role of immune inflammation in depression and provide a new clue for the diagnosis and treatment of this disorder. Notably, the multi‐omics approach employed in this study represents a pioneering effort in the field, providing unprecedented insights into the molecular mechanisms underlying depression.https://doi.org/10.1002/brb3.70549depressionproteomicsmetabolomicsmulti‐omics analysis
spellingShingle Wen‐Wen Li
Rui Xiao
Xue‐Yi Chen
Jun‐Cai Pu
Jian‐Jun Chen
Hai‐Yang Wang
Lan‐Xiang Liu
Dan Li
Yang‐Dong Zhang
Wen‐Xia Li
Peng Xie
Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
Brain and Behavior
depression
proteomics
metabolomics
multi‐omics analysis
title Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
title_full Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
title_fullStr Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
title_full_unstemmed Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
title_short Multi‐Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide‐Induced Mouse Model of Depression
title_sort multi omics analysis reveals disturbances of purine metabolism and glutamate metabolism in the hippocampus of lipopolysaccharide induced mouse model of depression
topic depression
proteomics
metabolomics
multi‐omics analysis
url https://doi.org/10.1002/brb3.70549
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