Dexmedetomidine attenuates sevoflurane‑induced neurocognitive impairment through &amp;alpha;2‑adrenoceptors

Zhang, Yufeng; Li, Mao; Cui, Enhui; Zhang, Hao; Zhu, Xiaozhong; Zhou, Jing; Yan, Ming; Sun, Jia

doi:10.3892/mmr.2020.11676

Cited by 17 publications

(14 citation statements)

References 38 publications

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“…As previously described, DEX is demonstrated to protect against anesthesia-induced neurotoxicity by several studies (Sanders et al, 2010). A recent study confirmed that DEX exerted neuroprotective effects by inhibiting sevoflurane-induced apoptosis, inflammation, and oxidative stress in P6 mice (Zhang et al, 2021). Neonatal injection of DEX can enhance spatial learning and memory in rat pups, potentially by promoting hippocampal neurogenesis and synaptic plasticity .…”

Section: Discussionmentioning

confidence: 64%

Role of NR2B/ERK signaling in the neuroprotective effect of dexmedetomidine against sevoflurane induced neurological dysfunction in the developing rat brain

Cao

Jin

et al. 2022

Acta Neurobiol. Exp.

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Dexmedetomidine (DEX) is a potent α-2 adrenergic receptor agonist and has been widely applied in clinic. The present study explored the protective effect of DEX on sevoflurane-induced learning and cognitive impairment and examined its underlying mechanism.Sprague-Dawley rat pups were exposed to 0.85% sevoflurane for 6 h and injected with DEX in different doses. The Morris water maze test was performed to evaluate the learning and memory function of rats. Western blot was used for the measurement of protein levels.The water maze results indicated that sevoflurane treatment increased the escape latency but reduced the time spent in the original quadrant of rats. The protein levels of NR2B, phosphorylated ERK were significantly influenced by sevoflurane. Ifenprodil administration alleviated sevoflurane-induced neurological impairment. DEX treatment reversed the effect of sevoflurane on both escape latency and time in original quadrant in a dose manner, and pretreatment with DEX had the most dramatic effect. DEX regulated the NR2B/ERK signaling in sevoflurane treated rats. NR2B/ERK signaling is involved in sevoflurane induced neurological impairment. DEX may protect against sevoflurane induced neurological dysfunction in the developing rat brain via regulating the NR2B/ERK signaling.

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Section: Discussionmentioning

confidence: 64%

Role of NR2B/ERK signaling in the neuroprotective effect of dexmedetomidine against sevoflurane induced neurological dysfunction in the developing rat brain

Cao

Jin

et al. 2022

Acta Neurobiol. Exp.

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“…[ 22 ] Besides, Dex attenuates Sev‐induced neurocognitive impairment through α2‐adrenoceptors. [ 23 ] In our study, we evaluated the effects of Dex on Sev‐induced neurotoxicity. Consistent with the previous studies, the treatment of Dex alleviated neuron apoptosis, pathological changes of the hippocampus, and the injury of learning and memory ability.…”

Section: Discussionmentioning

confidence: 99%

“…HSP60 was reported to act as a marker of mitophagy. [ 23 ] Therefore, we examined the expression of HSP60 in response to Dex treatment and the results indicated that HSP60 expression was increased by Dex treatment, implying that mitophagy was activated. LC3 is a typical marker of autophagy and the LC3II/I ratio is widely used to assess the level of autophagy.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine regulates sevoflurane‐induced neurotoxicity through the miR‐330‐3p/ULK1 axis

Xu¹,

Gao²,

Liang³

2021

J Biochem & Molecular Tox

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Sevoflurane (Sev), a widely used volatile anesthetic, can cause long‐term neurotoxicity and learning and memory impairment. Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects in numerous neurological disorders. Our work aimed to evaluate the molecular mechanisms of Dex in Sev‐induced neurotoxicity. In this study, it was found that Dex mitigated Sev‐induced neurotoxicity. Moreover, Sev treatment upregulated the miR‐330‐3p expression in hippocampus tissues, while this effect was reversed by the Dex treatment. Additionally, microRNA‐330‐3p (miR‐330‐3p) inhibition was verified to inhibit cell apoptosis and facilitate mitophagy. ULK1 was confirmed as a downstream target of miR‐330‐3p and miR‐330‐3p could negatively regulate ULK1 expression. Finally, the effects of miR‐330‐3p inhibition on Sev‐induced neurotoxicity could be offset by ULK1 knockdown or further intensified by Dex treatment. In summary, our study demonstrated that Dex regulated cell apoptosis and mitophagy in Sev‐induced neurotoxicity through the miR‐330‐3p/ULK1 axis. These findings might provide novel insights into the treatment of Sev‐induced neurotoxicity.

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“…Previous studies demonstrated that pretreatment with DEX could reduce learning and memory impairment, and decrease neuronal cell apoptosis, in ammation and oxidative stress. Moreover, the neuroprotective effects of DEX was reversed by yohimbine, an α2adrenoceptor antagonist, suggesting that the effects of DEX may be mediated by α2 adrenoceptors (13). DEX increases extracellular signal regulated kinases (ERK) ½ phosphorylation, a key mitogen-activated proteinkinase involved in cell survival and memory by the activation of proteinkinase C, andprobably imidazoline receptors (44,45).…”

Section: Cheng and Colleagues Using Whole Cell Patch Clamp Techniquementioning

confidence: 99%

“…DEX is an α2 adrenoceptor agonist that has been used as an anesthetic agent and sedative for several years (13). DEX produces dose-dependent sedation, anxiolysis, and analgesia without respiratory depression.…”

Section: Introductionmentioning

confidence: 99%

Comparing the Effect of Dexmedetomidine and Etomidate Administration with Acute Height Stress on Spatial Memory in Male Mice

Tarbiat

Rezaei

Emam

et al. 2021

Preprint

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Background: Nowadays, anesthetic drugs are widely used in anesthesia and surgical procedures and their effects on memory have been the focus of attention for a very long time. The effects of these common drugs include Dexmedetomidine (DEX) and Etomidate (ETO), on memory are controversial. In this study, the effects of these two drugs, co-administrated with heights stress, were evaluated on short-term and long-term spatial memory. 48 male mice were divided into 6 experimental groups consisting of Control, Control+heightstress (H.S), ETO, ETO+H.S, DEX+H.S. Drugs were administered Intra-peritoneal with doses of 0.3-0.4 mg/kg and 11 mg/kg for DEX and ETO respectively, and spatial memory was assessed using the Barnes Model.Results: DEX improved acquisition and retention of spatial reference memory, whereas ETO showed no such effects. In addition, DEX and ETO showed excitatory effects on short-term spatial memory, however DEX was more effective than ETO.Conclusion: the results suggested the neuoprotective, synaptic plasticity and memory improving effects of DEX on spatial reference and working memory. However, the precise neuronal and molecular mechanisms of these effects and their relation to the anti-stress system is still unknown and requires further research.

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Dexmedetomidine attenuates sevoflurane‑induced neurocognitive impairment through α2‑adrenoceptors

Cited by 17 publications

References 38 publications

Role of NR2B/ERK signaling in the neuroprotective effect of dexmedetomidine against sevoflurane induced neurological dysfunction in the developing rat brain

Role of NR2B/ERK signaling in the neuroprotective effect of dexmedetomidine against sevoflurane induced neurological dysfunction in the developing rat brain

Dexmedetomidine regulates sevoflurane‐induced neurotoxicity through the miR‐330‐3p/ULK1 axis

Comparing the Effect of Dexmedetomidine and Etomidate Administration with Acute Height Stress on Spatial Memory in Male Mice

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