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

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

PROVIDER: PRJNA1081874 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28152587_1.fastq.gz	Fastqsanger.gz
	SRR28152587_2.fastq.gz	Fastqsanger.gz
	SRR28152588_1.fastq.gz	Fastqsanger.gz
	SRR28152588_2.fastq.gz	Fastqsanger.gz
	SRR28152589_1.fastq.gz	Fastqsanger.gz

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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

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.

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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

Role of reducing Hmbox1 in cardiac ischemia/reperfusion injury

Project description:Role of reducing Hmbox1 in cardiac ischemia/reperfusion injury

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

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

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Role of reducing Hmbox1 in cardiac ischemia/reperfusion injury

Project description:This RNA-sequencing was performed to determine the differentially expressed mRNA after inhibition of Hmbox1 in cardiac ischemia/reperfusion injury

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Transcription profiling of white and grey matter in the distribution on the middle cerebral artery 6 hours after administration of the saline/catalytic antioxidant AEOL 10150 and ischemia/reperfusion of the MCAO to study the effect of AEOL 10150 on gene expression.

Project description:A catalytic antioxidant (AEOL 10150) attenuates expression of inflammatory genes in stroke. White and grey matter in the distribution on the middle cerebral artery 6 hours after administration of the saline/catalytic antioxidant AEOL 10150 and ischemia/reperfusion of the MCAO; pooled mRNA from 6 brains.

2007-12-15 | E-GEOD-63 | biostudies-arrayexpress

Single-Cell RNA Sequencing Unveils Lrg1's Role in Cerebral Ischemia‒Reperfusion Injury by Modulating Various Cells

Project description:Leucine-rich alpha-2 glycoprotein 1 (Lrg1) appears to be associated with the progression of cerebral ischemia-reperfusion injury, but its exact mechanism remains unknown. Here, we utilized scRNA-seq to compare the microenvironmental changes in the brains of Lrg1 knockout mice and wild-type mice following MCAO/R, in order to elucidate the role of Lrg1 after MCAO/R.

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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.

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Analysis of the effect of vascular endothelial growth factor on gene expression profile after focal cerebral ischemia in mouse

Project description:To investigate the effect of vascular endothelial growth factor (VEGF) on gene expression profile after focal cerebral ischemia in mouse, we employed Agilent SurePrint G3 Mouse Gene Expression 8M-CM-^W60K Microarray as a platform to identify which genes influenced by VEGF in mouse after focal cerebral ischemia. Mice were randomized to sham group, in which mice underwent sham surgery; MCAO group, in which transient (90 min) middle cerebral artery occlusion (MCAO) model was performed and mice received vehicle (PBS, 0.01M, pH 7.4) intracerebroventricularly in the right lateral ventricle 3hr after reperfusion; VEGF group (n = 36), in which rhVEGF-A165 (10M-NM-<g/ml, dissolved in 0.01M PBS) was injected into the right lateral ventricle 3hr after reperfusion. Mice were sacrificed at 24hr after reperfusion, brains removed and peri-infarct areas were used for microarray. Gene expression microarray was applied to investigate the differentially expressed genes among sham group, MCAO group and VEGF group. Expression of thirty-seven genes was confirmed in the same RNA samples by real-time PCR. Gene expression in sham group, MCAO group and VEGF group was measured at 24 hours after reperfusion. Three independent experiments were performed using different mice for each experiment.

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