ArticleExperimental brain research2023
The NR2B-targeted intervention alleviates the neuronal injuries at the sub-acute stage of cerebral ischemia: an exploration of stage-dependent strategy against ischemic insults.
Article in Experimental brain research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Baicalein-mediated regulation of Nrf2/ARE, NFĸB, and MAPK signaling in Huntington's disease: a promising strategy against neuroinflammation and neurodegeneration.Inflammopharmacology · 2025Review
- Role of phosphorylated Y1252, Y1336 and Y1472 on NR2B subunits in hypoxia tolerance of neuronal cell in vitro.Experimental brain research · 2024Article
- A potential role of gut microbiota in stroke: mechanisms, therapeutic strategies and future prospective.Psychopharmacology · 2024Review
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7 authors at 2 institutions in 2 countries.
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Abstract
Stroke is reported to be the second leading cause of death worldwide, among which ischemic stroke has fourfold greater incidence than intracerebral hemorrhage. Excitotoxicity induced by NMDAR plays a central role in ischemic stroke-induced neuronal death. However, intervention targeted NMDARs against ischemic stroke has failed, which may result from the complex composition of NMDARs and the dynamic changes of their subunits. In this current study, the levels of NR1, NR2A and NR2B subunits of NMDARs were observed upon different time points during the reperfusion after 1 h ischemia with the western blot assay. It was found that the changes of NR1 subunit were only detected after ischemia 1 h/reperfusion 1 day (1 d). While, the changes of NR2A and NR2B subunits may last to ischemia 1 h/reperfusion 7 day(7 d), indicating that NR2subunits may be a potential target for ischemia-reperfusion injuries at the sub-acute stage of ischemic stroke. Simultaneously, mitochondrial injuries in neurons were investigated with transmission electron microscopy (TEM), and mitochondrial dysfunction was evaluated with mitochondrial membrane proteins oxidative respiratory chain complex and OCR. When the antagonist of NMDARs was used before ischemic exposure, the neuronal mitochondrial dysfunction was alleviated, suggesting that these aberrant deviations of NMDARs from basal levels led to mitochondrial dysfunction. Furthermore, when the antagonist of NR2B was administrated intracerebroventricularly at the sub-acute cerebral ischemia, the volume of cerebral infarct region was decreased and the neural functions were improved. To sum up, the ratio of NR2B-containing NMDARs is vital for mitochondrial homeostasis and then neuronal survival. NR2B-targeted intervention should be chosen at the sub-acute stage of cerebral ischemia.
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