Metabolomics analysis of the hippocampus in a rat model of traumatic brain injury during the acute phase
| Autor: | Jiekun Luo, Tao Tang, Dandan Feng, Fei Zheng, Pengfei Li, Yang Wang, Yan-Tao Zhou |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Taurine
Nucleotidase activity hippocampus Traumatic brain injury protein database analysis Hypotaurine acute traumatic brain injury Bioinformatics 050105 experimental psychology lcsh:RC321-571 Pathogenesis 03 medical and health sciences Behavioral Neuroscience chemistry.chemical_compound 0302 clinical medicine Metabolomics Brain Injuries Traumatic medicine Animals 0501 psychology and cognitive sciences Databases Protein lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research business.industry 05 social sciences Carboxylic acid transmembrane transport Computational Biology Transporter Prognosis medicine.disease metabolomics Rats nervous system diseases Disease Models Animal nervous system chemistry Brain Injuries business Biomarkers 030217 neurology & neurosurgery |
| Zdroj: | Brain and Behavior, Vol 10, Iss 2, Pp n/a-n/a (2020) Brain and Behavior |
| ISSN: | 2162-3279 |
| DOI: | 10.1002/brb3.1520 |
| Popis: | Background Traumatic brain injury (TBI) has increased in rank among traumatic injuries worldwide. Traumatic brain injury is a serious obstacle given that its complex pathology represents a long‐term process. Recently, systems biology strategies such as metabolomics to investigate the multifactorial nature of TBI have facilitated attempts to find biomarkers and probe molecular pathways for its diagnosis and therapy. Methods This study included a group of 20 rats with controlled cortical impact and a group of 20 sham rats. We utilized mNSS tests to investigate neurological metabolic impairments on day 1 and day 3. Furthermore, we applied metabolomics and bioinformatics to determine the metabolic perturbation caused by TBI during the acute period in the hippocampus tissue of controlled cortical impact (CCI) rats. Notably, TBI–protein–metabolite subnetworks identified from a database were assessed for associations between metabolites and TBI by the dysregulation of related enzymes and transporters. Results Our results identified 7 and 8 biomarkers on day 1 and day 3, respectively. Additionally, related pathway disorders showed effects on arginine and proline metabolism as well as taurine and hypotaurine metabolism on day 3 in acute TBI. Furthermore, according to metabolite–protein database searches, 25 metabolite–protein pairs were established as causally associated with TBI. Further, bioinformation indicated that these TBI‐associated proteins mainly take part in 5′‐nucleotidase activity and carboxylic acid transmembrane transport. In addition, interweaved networks were constructed to show that the development of TBI might be affected by metabolite‐related proteins and their protein pathways. Conclusion The overall results show that acute TBI is susceptible to metabolic disorders, and the joint metabolite–protein network analysis provides a favorable prediction of TBI pathogenesis mechanisms in the brain. The signatures in the hippocampus might be promising for the development of biomarkers and pathways relevant to acute TBI and could further guide testable predictions of the underlying mechanism of TBI. Metabolomics was used to reveal the gain a metabolic perturbation of TBI in rats. Acute TBI was susceptible to metabolic disorders, and joint metabolite‐protein network analysis provides a favorable prediction to TBI pathogenesis mechanism in the brain. |
| Databáze: | OpenAIRE |
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