Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NMN ameliorates brain ischemia reperfusion injury after MCAO by reducing apoptosis and neutrophil extracellular trap formation in rats

ABSTRACT: NMN ameliorates brain ischemia reperfusion injury after MCAO by reducing apoptosis and neutrophil extracellular trap formation in rats

PROVIDER: PRJNA1172316 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30976379_1.fastq.gz	Fastqsanger.gz
	SRR30976379_2.fastq.gz	Fastqsanger.gz
	SRR30976380_1.fastq.gz	Fastqsanger.gz
	SRR30976380_2.fastq.gz	Fastqsanger.gz
	SRR30976381_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 19

Similar Datasets

NMN ameliorates brain ischemia reperfusion injury after MCAO by reducing apoptosis and neutrophil extracellular trap formation in rats

Project description:Ischemia reperfusion injury (IRI) is a common disease encountered in clinical practice, especially in the management of patients experiencing shock and the treatment of patients with cerebral infarction, and it is also an important factor in the poor prognosis of patients with cardiopulmonary resuscitation or stroke. Therefore, in this study, we constructed rat MCAO models and treated them with NMN. The tissues was collected for RNAseq to explore the gene expression and pathways influenced by NMN. We detected the neutrophil content by flow cytometry, apoptosis was detected by TUNEL staining and flow cytometry, the formation of NETs was evaluated by quantification of NE-DNA, and qPCR and Western blotting were performed to detect the expression of related genes. Our results showed there were fewer apoptotic cells after NMN treatment, and the ROS production was decreased. Importantly, the neutrophil was decreased and NETs were reduced after NMN treatment. Meanwhile, we observed the levels of p-ERK and p-p38 were decreased. Our findings indicated that NMN reduced cerebral ischemia reperfusion injury in rat MCAO model. NMN treatment decreased neutrophil and reduced NETs formation. The mechanism was referred to as the inhibition effect of ROS and ERK/p38 signaling.

2024-10-14 | GSE279377 | GEO

Hypidonehydrochloride (YL-0919) improves MCAO-induced ischemia-reperfusion injury by reducing inflammation

Project description:YL-0919 can alleviate the inflammatory response, reduce the area of cerebral infarction, decrease the degree of cell apoptosis on the injured side, hasten the regeneration of neurons, improve nerve function injury, and accelerate the recovery of motor function after MCAO surgery.

2025-02-11 | GSE260488 | GEO

Hypidonehydrochloride (YL-0919) improves MCAO-induced ischemia-reperfusion injury by reducing inflammation

Project description:Hypidonehydrochloride (YL-0919) improves MCAO-induced ischemia-reperfusion injury by reducing inflammation

| PRJNA1081874 | ENA

All-Trans Retinoic Acid Ameliorates Myocardial Ischemia/Reperfusion Injury by Reducing Cardiomyocyte Apoptosis.

Project description:Myocardial ischemia/reperfusion (I/R) injury interferes with the restoration of blood flow to ischemic myocardium. Oxidative stress-elicited apoptosis has been reported to contribute to I/R injury. All-trans retinoic acid (ATRA) has anti-apoptotic activity as previously reported. Here, we investigated the effects and the mechanism of action of ATRA on myocardial I/R injury both in vivo and in vitro. In vivo, ATRA reduced the size of the infarcted area (17.81±1.05% vs. 24.41±1.03%, P<0.05) and rescued cardiac function loss (ejection fraction 46.42±6.76% vs. 37.18±4.63%, P<0.05) after I/R injury. Flow-cytometric analysis and TUNEL assay demonstrated that the protective role of ATRA on myocardial I/R injury was related to its anti-apoptotic effects. The anti-apoptotic effects of ATRA were associated with partial inhibition of reactive oxygen species (ROS) production and significantly less phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, JNK, and ERK. Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 ± 0.20 vs. 0.41±0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 ± 0.17 vs. 0.52 ± 0.11 in vivo). Concomitantly, the protective role of ATRA on I/R injury was not observed in RAGE-KO mice. The current results indicated that ATRA could prevent myocardial injury and reduced cardiomyocyte apoptosis after I/R effectively. One possible mechanism underlying these effects is that ATRA could increase ADAM10 expression and thus cleave RAGE, which is the main receptor up-stream of MAPKs in myocardial I/R injury, resulting in the down-regulation of MAPK signaling and protective role on myocardial I/R injury.

| S-EPMC4506146 | biostudies-literature

Transcription profiling of mouse forebrain with induced middle cerebral artery occlusion (MCAO) to study permanent focal cerebral ischemia

Project description:profiling gene transcription in a mouse model of permanent focal cerebral ischemia that was induced by middle cerebral artery occlusion (MCAO)

2009-03-07 | E-TABM-655 | biostudies-arrayexpress

SWATH proteomics of NMN effects

Project description:Nicotinamide mononucleotide (NMN) has emerged as a promising therapeutic intervention for age-related disorders, including Type 2 Diabetes. In this study, we investigated the effects of NMN treatment on glucose uptake and its underlying mechanisms in mouse tissues (muscle, liver, brain and adipose tissue) and cell lines (HepG2 and C2C12). Through a comprehensive proteomic analysis, we uncovered a series of distinct organ-specific effects that contribute to the observed improvements in glucose metabolism.

2024-06-16 | PXD043257 | Pride

mRNA microarray in MCAo rat model with IV-hUMSC

Project description:To evaluate the change of gene expression at cerebral infarction by the treatment of IV-human umblical cord derived mesenchymal stem cell. RNA was isolated from the ipsilateral hemisphere to MCAo in rats. At 72 h post-MCAo, the ipsilateral hemisphere subjected to MCAo was used for mRNA microarray. RNA was isolated from the ipsilateral hemisphere to MCAo in rats without MCAo (control group, n=5), rats treated with 1x106 IV-hUMSC (hUMSC group, n=6) and saline (saline group, n=5) at 24h post-MCAo.

2017-03-01 | GSE78731 | GEO

Global gene expression profile of cerebral ischemia-reperfusion injury in rat MCAO model.

Project description:It is well-established that reperfusion following cerebral ischemic injury gives rise to secondary injury accompanied by structural and functional damage. However, it remains unclear how global genes changes in cerebral ischemia-reperfusion injury (IRI). This study investigated global gene expression in the hippocampi of Wistar rats following transient cerebral IRI using an RNA-sequencing strategy. The results revealed ≥2-fold up-regulation of 156 genes and ≥2-fold down-regulation of 26 genes at 24 h post-reperfusion. Fifteen differentially expressed genes were selected to confirm the RNA-sequencing results. Gene expression levels were dynamic, with the peak expression level of each gene occurring at different time points post-reperfusion. Gene Ontology (GO) analysis classified the differentially expressed genes as mainly involved in inflammation, stress and immune response, glucose metabolism, proapoptosis, antiapoptosis, and biological processes. KEGG pathway analysis suggested that IRI activated different signaling pathways, including focal adhesion, regulation of actin cytoskeleton, cytokine-cytokine receptor interaction, MAPK signaling, and Jak-STAT signaling. This study describes global gene expression profiles in the hippocampi of Wistar rats using the middle cerebral artery occlusion (MCAO) model. These findings provide new insights into the molecular pathogenesis of IRI and potential drug targets for the prevention and treatment of IRI in the future.

| S-EPMC5650366 | biostudies-literature

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

Dexmedetomidine preconditioning ameliorates kidney ischemia-reperfusion injury.

Project description:Kidney ischemia-reperfusion (I/R) injury is a common cause of acute kidney injury. We tested whether dexmedetomidine (Dex), an alpha2 adrenoceptor (α2-AR) agonist, protects against kidney I/R injury. Sprague-Dawley rats were divided into four groups: (1) Sham-operated group; (2) I/R group (40 min ischemia followed by 24 h reperfusion); (3) I/R group + Dex (1 μg/kg i.v. 60 min before the surgery), (4) I/R group + Dex (10 μg/kg). The effects of Dex postconditiong (Dex 1 or 10 μg/kg i.v. after reperfusion) as well as the effects of peripheral α2-AR agonism with fadolmidine were also examined. Hemodynamic effects were monitored, renal function measured, and acute tubular damage along with monocyte/macrophage infiltration scored. Kidney protein kinase B, toll like receptor 4, light chain 3B, p38 mitogen-activated protein kinase (p38 MAPK), sirtuin 1, adenosine monophosphate kinase (AMPK), and endothelial nitric oxide synthase (eNOS) expressions were measured, and kidney transciptome profiles analyzed. Dex preconditioning, but not postconditioning, attenuated I/R injury-induced renal dysfunction, acute tubular necrosis and inflammatory response. Neither pre- nor postconditioning with fadolmidine protected kidneys. Dex decreased blood pressure more than fadolmidine, ameliorated I/R-induced impairment of autophagy and increased renal p38 and eNOS expressions. Dex downregulated 245 and upregulated 61 genes representing 17 enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, in particular, integrin pathway and CD44. Ingenuity analysis revealed inhibition of Rac and nuclear factor (erythroid-derived 2)-like 2 pathways, whereas aryl hydrocarbon receptor (AHR) pathway was activated. Dex preconditioning ameliorates kidney I/R injury and inflammatory response, at least in part, through p38-CD44-pathway and possibly also through ischemic preconditioning.

| S-EPMC4186414 | biostudies-literature

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