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.
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.
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
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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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Posted 03 Mar, 2021
Received 19 Mar, 2021
On 13 Mar, 2021
On 07 Mar, 2021
Invitations sent on 27 Feb, 2021
On 26 Feb, 2021
On 25 Feb, 2021
On 25 Feb, 2021
Posted 03 Mar, 2021
Received 19 Mar, 2021
On 13 Mar, 2021
On 07 Mar, 2021
Invitations sent on 27 Feb, 2021
On 26 Feb, 2021
On 25 Feb, 2021
On 25 Feb, 2021
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.
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.
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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