ArticleImmunity, inflammation and disease2024
Dexmedetomidine activates the PKA/CREB pathway and inhibits proinflammatory factor expression through β2 adrenergic receptors.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- Article
- Dexmedetomidine administration is associated with a reduced risk of ICU mortality in critically ill patients with ischemic stroke.Frontiers in neurology · 2025Article
- Comparative Analysis of Volatile Components in Chi-Nan and Ordinary Agarwood Aromatherapies: Implications for Sleep Improvement.Pharmaceuticals (Basel, Switzerland) · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDexmedetomidine (DEX) is primarily utilized for sedation in the context of general anesthesia or intensive care. However, the exact regulatory mechanism by which DEX affects cytokines remains unclear. This study aims to investigate the underlying mechanism by which DEX inhibits proinflammatory factors through activation of the β2 adrenergic receptor (β2 AR).
methodsThe inflammatory cell model of human mononuclear macrophage (THP-1) cells induced by lipopolysaccharide (LPS) was established to study the effect of DEX on the expression of cell-related inflammatory factors. ADRA2A gene knockout THP-1 cells (THP-1
resultsThe results demonstrated a significant reduction in the expression levels of MCP-1, interleukin-06, and IL-8 in both THP-1 and THP-1
conclusionDEX initiates the activation of the PKA/CREB pathway through the activation of β2 AR. Simultaneously, it exerts an inhibitory effect on the activation of NF-κB, consequently reducing the transcription of proinflammatory factors while increasing the transcription of anti-inflammatory factors.
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