Dexmedetomidine prevents desflurane-induced motor neuron death through NF-KappaB pathway
| Autor: | Qingshan Ye, Danting Jia, Yun Wang, Longcai Dong, Xiaohong Zhou, Wenxun Liu |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Agonist medicine.drug_class Clinical Biochemistry Biochemistry Neuroprotection Lesion 03 medical and health sciences Desflurane Mice Structure-Activity Relationship 0302 clinical medicine medicine Animals Dexmedetomidine Maze Learning Cells Cultured Motor Neurons Cell Death Dose-Response Relationship Drug business.industry Neurotoxicity NF-kappa B Cell Biology General Medicine Motor neuron medicine.disease 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis medicine.symptom Neuron death business Neuroscience medicine.drug Signal Transduction |
| Zdroj: | Cell biochemistry and functionREFERENCES. 38(1) |
| ISSN: | 1099-0844 |
| Popis: | Desflurane is one of the commonly used general anaesthetics. Recently, it was reported that desflurane caused neurotoxicity, raising concerns in clinical use. In this study, we found desflurane could affect viability and maturation in motor neurons. Dexmedetomidine, a α2-adrenergic receptor agonist, could attenuate the effect of desflurane on motor neurons. This process was mediated by NF-KappaB signalling. Interestingly, we also found that dexmedetomidine could recover the lesion in motor function and memory impaired by desflurane. Collectively, our results showed the neurotoxic effect of desflurane in motor neurons. More importantly, this process was alleviated by dexmedetomidine, potentially showing its application in protecting motor neuron from neurotoxic agents. Significance of the study: This work provides the evidence to support the protective role of dexmedetomidine in desflurane-induced motor neuron death. Since desflurane is a widely used anaesthetic in surgery and leads to neuron death, the neuroprotective effect of dexmedetomidine holds promising clinical application. |
| Databáze: | OpenAIRE |
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