ArticleNeuropsychiatric disease and treatment2019
UPLC-Q-TOF-MS profiling of the hippocampus reveals metabolite biomarkers for the impact of Dl-3-n-butylphthalide on the lipopolysaccharide-induced rat model of depression.
Article in Neuropsychiatric disease and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Multi-Omics Analysis Reveals Disturbances of Purine Metabolism and Glutamate Metabolism in the Hippocampus of Lipopolysaccharide-Induced Mouse Model of Depression.Brain and behavior · 2025Article
- Dulaglutide treatment reverses depression-like behavior and hippocampal metabolomic homeostasis in mice exposed to chronic mild stress.Brain and behavior · 2024Article
- Metabolomic Profiling Reveals Biomarkers in Coronary Heart Disease Comorbidity.Journal of diabetes research · 2024Article
- Discovery of Biomarkers for Myogenous Temporomandibular Disorders Through Salivary Metabolomic Profiling: A Pilot Study.Journal of oral & facial pain and headache · 2023Article
- Paclitaxel Induces Neurotoxicity by Disrupting Tricarboxylic Acid Cycle Metabolic Balance in the Mouse Hippocampus.Journal of toxicology · 2023Article
- Dl-3-n-butylphthalide inhibits neuroinflammation by stimulating foxp3 and Ki-67 in an ischemic stroke model.Aging · 2021Article
- Comprehensive Evaluation of Lipopolysaccharide-Induced Changes in Rats Based on Metabolomics.Journal of inflammation research · 2020Article
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8 authors.
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Abstract
purposeAn increasing body of evidence reveals that inflammation is involved in the pathological mechanisms of depression. Our previous basic research confirmed that Dl-3-n-butylphthalide (NBP) possess anti-inflammatory properties. However, studies investigating metabolite biomarkers for the involvement of NBP in hippocampus tissue in the lipopolysaccharide (LPS)-induced rat model of depression are currently limited. Thus, the aim of this study was to identify metabolite biomarkers in the hippocampus for the impact of NBP in this model of depression. MATERIAL AND
methodsMale Sprague-Dawley rats were randomly allocated to one of the following three groups (n=6): Control, LPS-induced rat model of depression (LPS), and NBP involvement in the LPS-induced rat model of depression (LPS+NBP). Ultra-high-performance liquid chromatography-mass spectroscopy was used to determine the hippocampal metabolites. Multivariate statistical analysis was performed to identify differentially expressed hippocampal metabolites in the three groups.
resultsMost of the identified differentially expressed metabolites were related to amino acid, lipid, energy, and oxidative stress metabolism. Additionally, metabolites were eventually connected to different pathways and metabolic networks, which may partly account for the pathophysiological process of depression.
conclusionThe present findings provide insight into the anti-inflammatory effects of NBP, and further elucidate the pathophysiological mechanisms underlying inflammation-induced depression.
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