ArticleIranian journal of biotechnology2023
Dexmedetomidine Suppresses Glutamate-Stimulated Neuronal Injury Via MicroRNA-433/Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Pathway.
Article in Iranian journal of biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Glutamate and excitotoxicity in central nervous system disorders: ionotropic glutamate receptors as a target for neuroprotection.Neuroprotection (Chichester, England) · 2024Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cerebral ischemia has been a hotpot in the prevention and treatment of cerebral ischemia. Dexmedetomidine (Dex) is a new type of highly selective α2 adrenergic receptor agonist with pharmacological properties. Objective: Quantitative studies have shown that Dex has a protective effect on glutamate (Glu)-induced neuronal damage. however, its mechanism has not been fully elucidated. The purpose of this study was to explore the underlying molecular mechanism by which Dex ameliorates Glu-induced neuronal injury by regulating miR-433/JAK2/STAT3 axis. Materials and Methods: A model of neuronal injury was constructed by Glu treatment and intervened with Dex. miRNA expression profiling assay was conducted to screen potential miRNAs affected by Dex. Cell viability, lactate dehydrogenase (LDH) release and apoptosis were detected by MTT assay, LDH kit, and TUNEL staining, respectively. Oxidative stress indicators were assessed by ELISA whereas mitochondrial membrane potential (MMP) was assessed by C11-BODIPY581/591 staining. The targeting relationship between the miR-433 and JAK2 was verified by dual-luciferase reporter assay and gene expression was analyzed by quantitative PCR and Western blot. Results: Glu treatment decreased cell viability and MMP and promoted LDH release, apoptosis and oxidative damage. Glu-induced changes in neurons were reversed after Dex treatment through upregulating the miR-433 expression to block the activation of JAK2/STAT3 pathway. Conclusions: Dex protects against Glu-induced neuronal injury by regulating miR-433/JAK2/STAT3 pathway, which provides new insights into the treatment of neuronal injury.
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