Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic analysis of whole blood to investigate the therapeutic effects of nervonic acid on cerebral ischemia-reperfusion injury in rats

ABSTRACT: Proteomic analysis of whole blood to investigate the therapeutic effects of nervonic acid on cerebral ischemia-reperfusion injury in rats

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Xianyu Li

PROVIDER: PXD059362 | iProX | Wed Jan 01 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Proteomic analysis of whole blood to investigate the therapeutic effects of nervonic acid on cerebral ischemia-reperfusion injury in rats.

Li Qingqing Q Zhang Fengrong F Li Xianyu X Wang Qing Q

Frontiers in cell and developmental biology 20250128

<h4>Introduction</h4>Blood proteomics offers a powerful approach for identifying disease-specific biomarkers. However, no reliable blood markers are currently available for the diagnosis stroke. Nervonic acid (NA), a vital long-chain monounsaturated fatty acid found in mammalian nervous tissue, shows promising therapeutic potential in neurological disorders. This study aimed to develop a reliable methodology for whole blood proteomics to identify early warning biomarkers and evaluate drug treatm ...[more]

PMID: 39936033

Similar Datasets

Gene expression profile in cerebral ischemia-reperfusion injury of rat model

Project description:To reveal the alterations of mRNA profile in cerebral ischemia-reperfusion injury in rat. The SD rats were used to established the middle cerebral artery occlusion and reperfusion (MCAO/R) model. RNA-seq were performed to identify differences in gene expression.

2021-03-15 | GSE163614 | GEO

phosphoproteome of hippocampus after focal cerebral ischemia 1.5 h and reperfusion 24 h in mice

Project description:We obtained the profiles of neuronal phosphoproteome after cerebral ischemia and reperfusion by isolating mice hippocampus. Hippocampus combined from either nine sham or nine focal cerebral ischemia 1.5 h and reperfusion 24 h (IR) mice were lysed, digested, labeled with different TMT tags, then pooled and analyzed by LC/LC-MS/MS. In total, we quantified 7,865 phosphopeptides,179 phosphorylation sites of 129 proteins were upregulated and 843 phosphorylation sites of 494 proteins were downregulated in hippocampus during cerebral ischemia 2 h compare with sham operation.

2024-02-15 | PXD033851 | Pride

Transcriptome profiling of mRNAs in cortex of rats with cerebral ischemia and reperfusion

Project description:We analyzed transcriptomic characteristic of motor cortex from Sprague-Dawley rats brain with cerebral ischemia and reperfusion (CIR).

2024-01-12 | GSE222704 | GEO

Transcriptomic study on protective effects of Danhong Injection against cerebral ischemia/reperfusion-induced damage

Project description:This study compared the gene expression change of rat brain (cerebral ischemia reperfusion model) before and after Danhong injection treatment

2018-04-17 | GSE106680 | GEO

Exosomal miR-193b-3p derived from Astrocytes Protects Cerebral BBB Integrity after Cerebral Ischemia‒Reperfusion via TRPM2 Inhibition

Project description:To detect the miRNAs that have undergone significant changes after cerebral ischemia-reperfusion and clarify which miRNAs play a role in this pathological process.

2025-08-12 | GSE305148 | GEO

Therapeutic potential of microglial SMEK1 via regulation of H3 lysine 9 lactylation in cerebral ischemia-reperfusion injury

Project description:Immune responses and neuroinflammation occurring after acute ischemic stroke (AIS) are closely related to brain injury. Histone lactylation is a metabolic stress-related histone modification that participates in the pathogenesis of various diseases. However, the role of histone regulation in cerebral ischemic stroke remains unknown. In this study, a transient middle cerebral artery occlusion (tMCAO/R) model and an oxygen–glucose deprivation and reoxygenation (OGD/R) model were used to simulate in vivo/in vitro ischemia–reperfusion injury. The underlying mechanism of microglial histone lactylation was investigated using microglia-specific SMEK1-overexpressing mice and BV2 cells. The results showed that lactate overload resulted in elevated histone lactylation after AIS. Decreased SMEK1 expression in microglia after ischemic stroke was associated with increased lactate levels and subsequent neuroinflammation. Microglia-specific SMEK1 deficiency in microglia after ischemia can promote lactate production by inhibiting the pyruvate dehydrogenase kinase 3-pyruvate dehydrogenase (PDK3-PDH) pathway. Specifically, H3 lysine 9 lactylation (H3K9la) activated Ldha and Hif-1α transcription in microglia and promoted glycolysis. SMEK1-overexpressing mice exhibited better neurologic recovery after ischemic stroke than control mice. Mechanistically, we provided new evidence that microglial histone lactylation promoted glycolysis in ischemia‒reperfusion injury and elucidated the potential role of SMEK1 as an upstream regulatory molecule in histone lactylation after cerebral ischemia. According to our results, microglial SMEK1 may be potential therapeutic targets for AIS.

2025-01-02 | GSE283233 | GEO

Transcriptome profiling of mRNAs in cortex of rats with cerebral ischemia and reperfusion treated by acupuncture

Project description:We analyzed transcriptomic characteristic of motor cortex from Sprague-Dawley rats brain with cerebral ischemia and reperfusion (CIR) treated by acupuncture.

2024-01-12 | GSE222705 | GEO

Quantitative Analysis of sham and Cerebral Ischemia 1.5 h Reperfusion 24 h Transcriptomes in mouse hippocampus

Project description:The goals of this study are to compare hippocampus transcriptome profiling (RNA-seq) after Cerebral Ischemia 1.5 h Reperfusion 24 h in mouse stroke model

2024-02-10 | GSE202391 | GEO

Proteomic analysis of focal cerebral ischemia/reperfusion injury in rats

Project description:Stroke is a leading cause of mortality and long-term disability and ischemic stroke accounts for 87% of all strokes. Though timely recanalization of the occluded vessel is essential in the treatment of ischemic stroke, it is well known to cause ischemia-reperfusion (I/R) injury which result in neuronal cell death, brain tissue loss and severe neurological deficits. In this work, we employed a global proteomic approach to examine the changes of cerebral cortex proteins in rats undergoing acute and long-term I/R injury. In vivo middle cerebral artery occlusion (MCAO) model of focal cerebral I/R injury in rats was established. The animals were divided into three model groups with 2 h-MCAO followed with different reperfusion time, 1 day, 7 days and 14 days, respectively. For each model group a sham group was correspondingly set. Each group included four animals. For proteomic analysis, cerebral cortex proteins were extracted and analyzed by SDS-PAGE, whole-lane slicing, in-gel digestion and label-free quantitative LC-MS/MS. A total of 5621 proteins were identified and their quantities between the surgery and corresponding sham groups and across the three reperfusion time points were compared for mechanism investigation. This dataset includes all the raw files of the 840 LC-MS runs (6 groups x 4 animals x 35 gel squares/sample), as well as their identification and quantitation results at the levels of peptide fragments, peptides and proteins, respectively.

2019-07-03 | PXD012151 | Pride

Long-Term Gene Expression Dynamics at the Neurovascular Unit After Cerebral Ischemia/Reperfusion Injury in Mice

Project description:With increasing distribution of endovascular stroke therapies, transient middle cerebral artery occlusion in mice depicts a relevant patient population with recanalized M1 occlusion. This study provides a well-controlled transcriptome dataset of short and long-term transcriptomic changes at the neurovascular unit in cerebral ischemia/reperfusion injury.

2020-03-10 | GSE131193 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data