ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2022
Dexmedetomidine pretreatment alleviates cerebral ischemia/reperfusion injury by inhibiting neuroinflammation through the JAK2/STAT3 pathway.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis.Advances in experimental medicine and biology · 2023Pooled it
- Effect of dexmedetomidine on liver transplantation: a meta-analysis.Frontiers in pharmacology · 2023Pooled it
- Sedation in Acute Ischemic Stroke: Pathophysiological Basis and Evidence for Commonly Used Agents.Translational stroke research · 2026Review
- Neuroprotective mechanisms of dexmedetomidine in perioperative neurocognitive disorders: From molecular pathways to clinical translation.Journal of anesthesia and translational medicine · 2025Review
- Article
- Adenosine A1 receptor agonist alleviates cerebral ischemia/reperfusion injury by inhibiting Nrf2/NLRP3 signaling‑mediated pyroptosis.Experimental and therapeutic medicine · 2025Article
- Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.Metabolic brain disease · 2025Article
- Study on the mechanism of Dexmedetomidine's effect on postoperative cognitive dysfunction in elderly people.Frontiers in physiology · 2025Review
- The Role of Intravenous Anesthetics for Neuro: Protection or Toxicity?Neuroscience bulletin · 2025Review
- Anesthetics in pathological cerebrovascular conditions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- Dexmedetomidine decreases cerebral hyperperfusion syndrome incidence following mechanical thrombectomy in acute ischemic stroke: a double-blind, randomized controlled trial.Frontiers in neurology · 2025Article
- Dexmedetomidine on the interplay of IL-6 and STAT3 pathways in adrenal gland damage-induced scalding burns in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Progress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.Brain and behavior · 2024Review
- Article
- EGFR-Activated JAK2/STAT3 Pathway Confers Neuroprotection in Spinal Cord Ischemia-Reperfusion Injury: Evidence from High-Throughput Sequencing and Experimental Models.Molecular neurobiology · 2024Article
- Bioinformatics analysis of genomic and immune infiltration patterns in autism spectrum disorder.Annals of translational medicine · 2022Article
- Research progress on molecular mechanisms of general anesthetic-induced neurotoxicity and cognitive impairment in the developing brain.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dexmedetomidine (DEX) is known to provide neuroprotection against cerebral ischemia and reperfusion injury (CIRI), but the exact mechanisms remain unclear. This study was conducted to investigate whether DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation through the JAK2/STAT3 signaling pathway. Middle cerebral artery occlusion (MCAO) was performed to establish a cerebral ischemia/reperfusion (I/R) model. Specific-pathogen-free male Sprague-Dawley rats were randomly divided into Sham, I/R, DEX, DEX+IL-6, and AG490 (a selective inhibitor of JAK2) groups. The Longa score, TTC staining, and HE staining were used to evaluate brain damage. ELISA was used to exam levels of TNF-α. Western blotting was used to assess the levels of JAK2, phosphorylated-JAK2 (p-JAK2), STAT3, and phosphorylated-STAT3 (p-STAT3). Our results suggested that both pretreatment with DEX and AG490 decreased the Longa score and cerebral infarct areas following cerebral I/R. After treatment with IL-6, the effects of DEX on abrogating these pathological changes were reduced. HE staining revealed that I/R-induced neuronal pathological changes were attenuated by DEX application, consistent with the AG490 group. However, these effects of DEX were abolished by IL-6. Furthermore, TNF-α levels were significantly increased in the I/R group, accompanied by an increase in the levels of the p-JAK2 and p-STAT3. DEX and AG490 pretreatment down-regulated the expressions of TNF-α, p-JAK2, and p-STAT3. In contrast, the down-regulation of TNF-α, p-JAK2, and p-STAT3 induced by DEX was reversed by IL-6. Collectively, our results indicated that DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation via negatively regulating the JAK2/STAT3 signaling pathway.
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