ArticleExperimental brain research2021
Investigation of brain damage mechanism in middle cerebral artery occlusion/reperfusion rats based on i-TRAQ quantitative proteomics.
Article in Experimental brain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- High-Resolution Spatiotemporal Mapping of Cerebral Metabolism During Middle-Cerebral-Artery Occlusion/Reperfusion Progression: Preliminary Insights.Biomolecules · 2025Article
- Identification of a novel pathogenic gene, NDUFA3, in Leigh Syndrome through whole exome sequencing.Neurogenetics · 2024Article
- HDAC/H3K27ac-mediated transcription of NDUFA3 exerts protective effects on high glucose-treated human nucleus pulposus cells through improving mitochondrial function.Scientific reports · 2024Article
- Proteomic analysis of Biliverdin protected cerebral ischemia-reperfusion injury in rats.Scientific reports · 2023Article
- Transcriptomics and metabolomics study in mouse kidney of the molecular mechanism underlying energy metabolism response to hypoxic stress in highland areas.Experimental and therapeutic medicine · 2023Article
- The Effect of N6-Methyladenosine Regulators and m6A Reader YTHDC1-Mediated N6-Methyladenosine Modification Is Involved in Oxidative Stress in Human Aortic Dissection.Oxidative medicine and cellular longevity · 2023Article
- A 69 kb Deletion in chr19q13.42 includingJournal of clinical medicine · 2022Article
- Molecular mechanisms for the prevention and promoting the recovery from ischemic stroke by nutraceutical laminarin: A comparative transcriptomic approach.Frontiers in nutrition · 2022Article
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12 authors at 1 institution in 1 country.
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Abstract
The objective of this study is to analyze the differential protein expression profile in cerebral cortex of rats with middle cerebral ischemia/reperfusion (MCAO/R), explore the brain damage mechanism of MCAO/R at protein level, and provide experimental foundation for searching specific marker proteins of MCAO/R. Rat model of MCAO/R was established by modified suture-occluded method, and the model was evaluated by the results of brain 2,3,5-triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (HE) staining. Cerebral cortex of rats from sham-operated group (Sham) and MCAO/R groups was used for FASP enzymatic hydrolysis, i-TRAQ quantitative labeling, and reverse-phase liquid chromatography purification and separation. Orbitrap Q Exactive mass spectrometry was used for qualitative and quantitative analyses of total differential protein expression profiles. MCAO/R rats had obvious cerebral infarction lesions, and the relative surface area of cerebral infarction was significantly different compared with sham rats, suggesting that MCAO/R rat model was successfully prepared. There were 199 significant difference proteins (MCAO/R vs Sham, p < 0.05, |fold change|> 1.2), including 104 up-regulated proteins and 95 down-regulated proteins. Gene ontology (GO) enrichment analysis showed that the up-regulated proteins were mainly concentrated in the biological processes of positive regulation of NF-κB transcription and I-κB kinase-NF-κB, etc. Down-regulated proteins were mainly concentrated in long-term synaptic potentiation, cellular response to DNA damage stimulus, etc. KEGG pathway analysis showed that the pathway involved in differential proteins includes oxidative phosphorylation, metabolic pathway, and Ras signaling pathway. Network analysis of differential proteins showed that Alb, ndufb5, ndufs7, ApoB, Cdc42, Ndufa3, Igf1r, P4hb, Mbp, Gc, Nme1, Akt2, and other proteins may play an important role in regulating oxidative stress, apoptosis, and inflammatory response in MCAO/R. Quantitative proteomics based on i-TRAQ labeling reveals the effect of inflammation and apoptosis in brain damage mechanism of MCAO/R. Besides, this research provide some experimental foundation for search and determination of potential therapeutic targets of MCAO/R.
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