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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE260488 | GEO | 2025/02/11

REPOSITORIES: GEO

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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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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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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.

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

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