ArticleIn vivo (Athens, Greece)
Dexmedetomidine Up-regulates Brain-derived Neurotrophic Factor
Article in In vivo (Athens, Greece). 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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Who cites it
1 citing paper in PubMed.
- Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology.Frontiers in molecular neuroscience · 2026Article
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5 authors.
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Abstract
BACKGROUND/
aimThe middle cerebral artery occlusion (MCAO) model is widely used to study stroke pathobiology. Dexmedetomidine (DEX) has demonstrated neuroprotective effects in ischemic brain models. Previous studies have shown that nuclear factor erythroid 2-related factor 2 (Nrf2) expression changes in the parietal cortex, which is supplied by the middle cerebral artery, after ischemic injury. While Nrf2 is known to regulate brain-derived neurotropic factor (BDNF) expression, its role in MCAO conditions has not been fully explored. This study aimed to investigate the effects of DEX on Nrf2 and BDNF expression in the parietal cortex following MCAO. MATERIALS AND
methodsMice were subjected to MCAO by inserting a silicone-coated suture into the common carotid artery. After 30 min, the suture was withdrawn to induce ischemia/reperfusion (IR) injury. Cortical brain tissues were harvested three days post-injury. Western blot analysis was performed to measure BDNF protein expression. The expression levels of the messenger ribonucleic acid (mRNA) Nrf2, pro-apoptotic protein (Bax), and anti-apoptotic protein (Bcl-2) were analyzed using quantitative real-time polymerase chain reaction.
resultsThe mRNA level of Nrf2 was significantly higher in the DEX group than in the MCAO group after three days of MCAO. BDNF protein expression (15 kDa) was also higher in the DEX group than in the MCAO group. Furthermore, Bax mRNA was lower, while Bcl-2 mRNA was higher in the DEX group than in the MCAO group.
conclusionDEX treatment up-regulated Nrf2 expression, which was associated with increased BDNF expression three days after MCAO.
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