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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

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			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

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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

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Beta-Hydroxybutyrate but not NMN supplementation mimics caloric restriction reducing early mortality in Daphnia

Project description:NAD+ homeostasis is an important determinant of lifespan and may be a key mechanism of caloric restriction (CR) expansion of lifespan. Ketone bodies such as beta-hydroxybutyrate (BHB) that regulate NAD+ abundance and NAD+ precursors such nicotinamide mononucleotide (NMN), are known to extend life in experimental animals and ameliorate age-related conditions in humans. We tested the hypothesis that chronic BHB and NMN exposure can extend lifespan similarly to the effect of CR treatment in a model organism Daphnia, a freshwater zooplankton crustacean. We also measured fecundity, lipofuscin accumulation, and lipid investments into offspring in Daphnia fed the full diet, full diet with BHB, NMN, and combined treatments, and fed the CR diet (25% of the full diet). We show that BHB exposure, but not NMN exposure, reduces early life mortality in fully fed Daphnia to levels similar to those observed under CR without compromising fecundity. We also observed that in a combined exposure cohort, NMN nearly eliminates the beneficial effect of BHB. None of the treatments affected lipofuscin accumulation, but the NMN and the combined treatment mimicked the effect of CR on neonate size in older females. An RNAseq experiment comparing the two diets and the two exposure treatments showed showed that BHB-treated Daphnia change expression of a variety of genes, including genes with known longevity extending effects, but differential expression of few genes is consistent with the effects of CR and their functionality is not clear.

2025-12-11 | GSE292526 | GEO

Acteoside ameliorates cerebral ischemia/reperfusion injury in MCAO rats as a natural plasma Kallikrein inhibitor from Osmanthus fragrans flower.

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CD11b Blockade Ameliorates Myocardial Ischemia/Reperfusion Injury by Reducing Neutrophil and Monocyte Infiltration.

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

Project description: Not available

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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.

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Prussian Blue Scavenger Ameliorates Hepatic Ischemia-Reperfusion Injury by Inhibiting Inflammation and Reducing Oxidative Stress.

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