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Research Article
huanqi Liu
Qingdao Agricultural University
Corresponding Author
License:
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Background
Dexmedetomidine (Dex) has a significant neuroprotective effect in isoflurane-induced neurotoxicity during the critical period of synaptogenesis. However, the mechanisms by which Dex protects developing neurons are not clear. This research evaluated the protective effect of Dex against neuronal damage induced by isoflurane using a mouse model.
Methods
Neonatal Swiss mice at postnatal day 7 (PND7) were injected intraperitoneally with 15µg/kg, 20µg/kg, or 25µg/kg Dex, or normal saline, and then treated with 2% isoflurane for 2h. The results showed that 20µg/kg Dex could reduce isoflurane-induced neurocognitive deficits as assessed using the Morris water maze. The mechanisms by which Dex protected neurons were investigated using hippocampal neurons isolated from PND4-7 mice and exposed to 2% isoflurane (2h). Dex prevented cytoskeletal depolymerization that was induced by isoflurane.
Results
15µg/ml Dex significantly reduced the percentage of apoptotic neurons. Dex reduced expression of activated caspase-3 in neurons compared to isoflurane only exposed mice. Using primary cell cultures from neonatal mouse hippocampi, we determined that dexmedetomidine could reverse isoflurane-induced RhoA (a small
Keywords
Dexmedetomidine, Neurotoxicity, BDNF, Neurocognitive, Actin Cytoskeleton
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The effects isoflurane on the cultured primary neurons. A, the actin cytoskeleton of cultured primary neurons treated with different concentration of isoflurane. F-actin was stained using TRITC-phalloidin. B, the effects of isoflurane on the expression of caspase-3 protein in hippocampal neurons. The results showed that both 1.5% and 2% of isoflurane could induce the actin cytoskeleton depolymerization and neuron apoptosis in hippocampal neurons compared to control group.
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CURRENT STATUS: Under Review
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Posted 03 Mar, 2021
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Review #1 received
Received 19 Mar, 2021
Reviewer #2 agreed
On 13 Mar, 2021
Reviewer #1 agreed
On 07 Mar, 2021
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Invitations sent on 27 Feb, 2021
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On 26 Feb, 2021
Editor invited
On 25 Feb, 2021
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On 25 Feb, 2021
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Subject Areas
Anesthesiology & Pain Medicine
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This preprint is under consideration at BMC Anesthesiology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
huanqi Liu
Qingdao Agricultural University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 03 Mar, 2021
No community comments so far
Review #1 received
Received 19 Mar, 2021
Reviewer #2 agreed
On 13 Mar, 2021
Reviewer #1 agreed
On 07 Mar, 2021
Reviewers invited
Invitations sent on 27 Feb, 2021
Submission checks complete
On 26 Feb, 2021
Editor invited
On 25 Feb, 2021
Editor assigned
On 25 Feb, 2021
Subject Areas
Anesthesiology & Pain Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Dexmedetomidine (Dex) has a significant neuroprotective effect in isoflurane-induced neurotoxicity during the critical period of synaptogenesis. However, the mechanisms by which Dex protects developing neurons are not clear. This research evaluated the protective effect of Dex against neuronal damage induced by isoflurane using a mouse model.
Methods
Neonatal Swiss mice at postnatal day 7 (PND7) were injected intraperitoneally with 15µg/kg, 20µg/kg, or 25µg/kg Dex, or normal saline, and then treated with 2% isoflurane for 2h. The results showed that 20µg/kg Dex could reduce isoflurane-induced neurocognitive deficits as assessed using the Morris water maze. The mechanisms by which Dex protected neurons were investigated using hippocampal neurons isolated from PND4-7 mice and exposed to 2% isoflurane (2h). Dex prevented cytoskeletal depolymerization that was induced by isoflurane.
Results
15µg/ml Dex significantly reduced the percentage of apoptotic neurons. Dex reduced expression of activated caspase-3 in neurons compared to isoflurane only exposed mice. Using primary cell cultures from neonatal mouse hippocampi, we determined that dexmedetomidine could reverse isoflurane-induced RhoA (a small
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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