Dexmedetomidine Reduces the Lidocaine-Induced Neurotoxicity by Inhibiting Inflammasome Activation and Reducing Pyroptosis in Rats

• Published in: Biological & pharmaceutical bulletin Vol. 44; no. 7; pp. 902 - 909
• Main Authors: Zhao, Guang-yi, Cao, Yan-yan, Ding, Xu-dong, Li, Lu
• Format: Journal Article
• Language: English
• Published: Japan The Pharmaceutical Society of Japan 01.07.2021; Pharmaceutical Society of Japan; Japan Science and Technology Agency
• Subjects: Adrenergic alpha-2 Receptor Agonists - pharmacology; Adrenergic alpha-2 Receptor Agonists - therapeutic use; Anesthetics, Local; Animals; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Apoptosis; Caspase-1; dexmedetomidine; Dexmedetomidine - pharmacology; Dexmedetomidine - therapeutic use; inflammasome; Inflammasomes; Inflammasomes - metabolism; Inflammation; Interleukin 18; Kinases; Lidocaine; Male; Microglia; Neurons - drug effects; Neuroprotection; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurotoxicity; Neurotoxicity Syndromes - drug therapy; Neurotoxicity Syndromes - metabolism; Phosphorylation; Phosphorylation - drug effects; Protein kinase C; Protein Kinase C-delta - metabolism; Pyroptosis; Pyroptosis - drug effects; Rats; Rats, Sprague-Dawley; Spinal Cord - drug effects; Spinal Cord - metabolism; Spinal cord injuries; pyroptosis; caspase 1; dexmedetomidine; inflammasome

Local anesthetic toxicity is closely related to neuronal death and activation of the inflammatory response. Dexmedetomidine (Dex) is an adrenergic α2 receptor agonist that can reduce the neurotoxicity induced by lidocaine. It also has anti-inflammatory effects. However, the mechanism underlying the...