ArticleJournal of inflammation research2022
Dexmedetomidine Activates Akt, STAT6 and IRF4 Modulating Cytoprotection and Macrophage Anti-Inflammatory Phenotype Against Acute Lung Injury in vivo and in vitro.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Effects of Esketamine-Dexmedetomidine Combination on Immediate Postprocedural Oxygenation Index in Severe Pneumonia Patients Undergoing Bedside Fiberoptic Bronchoscopic Sputum Aspiration: A Prospective Randomised Controlled Trial.Drug design, development and therapy · 2025Trial
- Co-localization of TAZ and H2A.Z up-regulates IL-6 expression in alveolar epithelial cells to polarize M2 cells to alleviate hypoxia-induced lung injury.Genes & diseases · 2026Article
- Sedation as an Immunomodulator of Inflammatory Responses in the Lung-Brain Axis of ARDS.International journal of molecular sciences · 2026Review
- Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers.Scientific reports · 2026Article
- Macrophage polarization in hematologic cancers: mechanisms and therapeutic strategies.Blood research · 2026Review
- Dexmedetomidine relieves LPS-induced acute lung injury by boosting HIF-1a/ACOD1 driven anti-inflammatory macrophage polarization.Genes and immunity · 2025Article
- Alveolar macrophages polarization switch via αInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- The regulatory role of dexmedetomidine in NLRP3 inflammasome-related organ protection.Journal of anesthesia and translational medicine · 2024Review
- ITGAM-macrophage modulation as a potential strategy for treating neutrophilic Asthma: insights from bioinformatics analysis and in vivo experiments.Apoptosis : an international journal on programmed cell death · 2024Article
- From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis.Frontiers in microbiology · 2024Review
- Dexmedetomidine regulates exosomal miR-29b-3p from macrophages and alleviates septic myocardial injury by promoting autophagy in cardiomyocytes via targeting glycogen synthase kinase 3β.Burns & trauma · 2024Article
- Regulated cell death and inflammasome activation in gut injury following traumatic surgery in vitro and in vivo: implication for postoperative death due to multiorgan dysfunction.Cell death discovery · 2023Article
- Review
- Intestinal homeostasis in the gut-lung-kidney axis: a prospective therapeutic target in immune-related chronic kidney diseases.Frontiers in immunology · 2023Review
- Agmatine suppresses the imidazoline IInternational journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aims to investigate the cytoprotective and anti-inflammatory effects of an α Methods: C57BL/6 mice were intraperitoneally injected LPS (10 mg/kg) with or without Dex (25 µg/kg) and/or α Results: Dex treatment significantly reduced pro-inflammatory M1 macrophage polarization and NLRP3 inflammasome activation in the lungs relative to the mice treated with LPS. The similar pattern reduction of NLRP3 inflammasome activation by Dex was also found in A549 cells. Atip partly reversed the anti-inflammatory effects of Dex. In cultured alveolar macrophages, Dex reduced LPS-mediated expression of IL-1, -6 and TNF-α receptors while promoting alveolar macrophages differentiation towards a M2 anti-inflammatory phenotype. Additionally, LPS increased Akt signaling activation in a time-dependent manner, which was further activated by Dex via inhibiting phosphatase and tensin homolog (PTEN). The action of Dex on Akt signaling shifted alveolar macrophages from M1 to M2 phenotype through increasing STAT6 and IRF4 transcriptional factors. Conclusion: Dex protected against LPS-induced lung injury and suppressed LPS-induced pulmonary inflammatory responses by attenuating the NLRP3 inflammasome activation and promoting anti-inflammatory M2 macrophage polarization.
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