ArticleNeurochemical research2022
MiR-665 Participates in the Protective Effect of Dexmedetomidine in Ischemic Stroke by ROCK2/NF-κB Axis.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury.Frontiers in immunology · 2022Pooled it
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- Progress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.Brain and behavior · 2024Review
- Article
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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
Ischemic stroke is a grievous intimidation to the healthiness of sufferers. Previous studies have reported that dexmedetomidine (DEX) has a protective effect on a variety of organs. This paper aimed to explore the regulatory mechanism of DEX in ischemic stroke through miR-665/ROCK2 axis. The mice model of ischemic stroke was constructed by middle cerebral artery occlusion (MCAO). The cell model of ischemic stroke was constructed by oxygen-glucose deprivation (OGD). Cell viability and apoptosis were assessed by CCK-8 assay and flow cytometry. The expression of cytokines was detected by ELISA. Lactate dehydrogenase (LDH) concentration was evaluated by LDH kit. The cerebral infarct volume of MCAO mice was detected by TTC staining, and the apoptosis of brain cells was detected by TUNEL staining. The target relationship between ROCK2 and miR-665 was analyzed by dual-luciferase reporter assay. DEX contributed cell viability from 42 to 66% (1 μM) and restrained cell apoptosis from 26 to 18% in HT22 cells treated with OGD (P < 0.01). Meanwhile, DEX decreased the expression of cytokines and LDH concentration from 184 to 126% (P < 0.001). Moreover, the expression of miR-665 enhanced 2.9 times (P < 0.05) and the expression of ROCK2 (P < 0.05) and NF-κB p65 (P < 0.01) reduced 1.8 times and 2.2 times after DEX treatment in OGD induced HT22. And miR-665 knockdown attenuated the effect of DEX on inflammation damage (the levels of TNF-α, IL-1β and IL-6 increased 1.36 times, 1.31 times, 1.43 time, respectively, and IL-10 decreased 1.68 times) and apoptosis from 17 to 25% (P < 0.01). MiR-665 directly targeted ROCK2 and regulated ROCK2 and NF-κB p65 expression (P < 0.01). Furthermore, ROCK2 overexpression inhibited the protective effect of DEX in HT22 induced by OGD (P < 0.001), while miR-665 overexpression reversed the regulatory of ROCK2 (P < 0.01). In vivo, DEX decreased cerebral infarction volume and inhibited apoptosis of brain cell (P < 0.001). DEX has a protective effect in ischemic stroke by promoting miR-665 expression to downregulate ROCK2/NF-κB axis, suggesting DEX has a beneficial effect on ischemic stroke and miR-665 is a conceivable target for the therapeutics and diagnosis of ischemic stroke.
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