ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Dexmedetomidine Post-Conditioning Alleviates Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting High Mobility Group Protein B1 Group (HMGB1)/Toll-Like Receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- 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
- Progress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.Brain and behavior · 2024Review
- Evaluation of SBDP145, melatonin, sLOX-1, HMGB1 and HIF-1α in preterm infants with brain injury.Italian journal of pediatrics · 2024Article
- Article
- Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases.Current drug targets · 2024Review
- MicroRNA-323-5p Involved in Dexmedetomidine Preconditioning Impart Neuroprotection.Medicina (Kaunas, Lithuania) · 2023Article
- Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway.Acta biochimica et biophysica Sinica · 2023Article
- Dexmedetomidine protects cells from Angiotensin II-induced smooth muscle cell phenotype switch and endothelial cell dysfunction.Cell cycle (Georgetown, Tex.) · 2023Article
- Stroke: Molecular mechanisms and therapies: Update on recent developments.Neurochemistry international · 2023Review
- Comparison of the effects of remimazolam and dexmedetomidine on early postoperative cognitive function in elderly patients with gastric cancer.Frontiers in aging neuroscience · 2023Article
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Electrocardiographic and histopathological characterizations of diabetic cardiomyopathy in rats.Environmental science and pollution research international · 2022Article
- Neuroinflammation in perioperative neurocognitive disorders: From bench to the bedside.CNS neuroscience & therapeutics · 2022Review
- Clinical Observation of Salvianolic Acid Combined with Panax Notoginseng Saponins Combined with Basic Nursing Intervention on Cerebral Ischemia-Reperfusion Injury in Rats.Journal of healthcare engineering · 2022Article
- Ischemic stroke: From pathological mechanisms to neuroprotective strategies.Frontiers in neurology · 2022Review
- Muscone improves hypoxia/reoxygenation (H/R)-induced neuronal injury by blocking HMGB1/TLR4/NF-κB pathwayPeerJ · 2022Article
- Ginsenoside Rh2 Inhibits NLRP3 Inflammasome Activation and Improves Exosomes to Alleviate Hypoxia-Induced Myocardial Injury.Frontiers in immunology · 2022Article
- Pinoresinol diglucoside alleviates ischemia/reperfusion-induced brain injury by modulating neuroinflammation and oxidative stress.Chemical biology & drug design · 2021Article
- Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Cerebral ischemia-reperfusion injury is a pivotal cause of deaths due to cerebrovascular accident. Increased research efforts are needed to reveal the mechanism underlying its aggravation or alleviation. In this study, the effects of dexmedetomidine post-conditioning on the HMGB1/TLR4/NF-kappaB signaling pathway in cerebral ischemia-reperfusion rats was explored. MATERIAL AND METHODS Ninety rats were randomly divided into 5 groups - a sham group (Sham), a model group (I/R), a dexmedetomidine post-conditioning group (Dex), a recombinant high mobility group protein B1 group (rHMGB1), and a recombinant HMGB1+dexmedetomidine post-conditioning group (rHMGB1+Dex) - with 18 rats in each group. Longa grading, wet-dry weighing, TTC staining, HE staining, and immunohistochemical staining were used to assess brain damage. ELISA, RT-PCR, and Western blot analyses were performed to assess expression of IL-1ß, TNF-alpha, IL-6, IL-8, HMGB1, TLR4, and NF-kappaB. RESULTS Compared with the I/R group, the neurological function score, brain water content, infarction area, and the number of COX-2- and IBA-1-positive cells in the Dex group were significantly lower, accompanied by downregulated expression of the HMGB1/TLR4/NF-kappaB pathway, alleviated inflammation, and oxidative stress injury in brain tissue. These trends were mostly reversed in the rHMGB1 group and rHMGB1+Dex group, but not in the Dex group. Furthermore, when compared to the Dex group, there were significant increases of H₂O₂, MDA, NO, IL-1ß, TNF-alpha, IL-6, IL-8, HMGB1, TLR4, and p-P65 in the rHMGB1 group and rHMGB1+Dex group, in which a significant decrease of T-AOC, SOD, and p-IkappaBalpha was also detected. CONCLUSIONS Dexmedetomidine post-conditioning can alleviate cerebral ischemia-reperfusion injury in rats by inhibiting the HMGB1/TLR4/NF-kappaB signaling pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.