ArticleFrontiers in cellular neuroscience2017
Upregulation of Cdh1 Attenuates Isoflurane-Induced Neuronal Apoptosis and Long-Term Cognitive Impairments in Developing Rats.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanisms of natural compounds in treating inhalation anesthesia-induced cognitive dysfunction.Frontiers in pharmacology · 2026Review
- Inhibition of Rac1 Attenuated Propofol-Induced Neurotoxicity in the Hippocampal Dentate Gyrus in Developing Mice.Neurochemical research · 2025Article
- Decoding the neurotoxic effects of propofol: insights into the RARα-Snhg1-Bdnf regulatory cascade.American journal of physiology. Cell physiology · 2024Article
- Hippocampal differential expression underlying the neuroprotective effect of delta-9-tetrahydrocannabinol microdose on old mice.Frontiers in neuroscience · 2023Article
- Effects of General Anesthetics on Synaptic Transmission and Plasticity.Current neuropharmacology · 2022Review
- CHIP Decline Is Associated With Isoflurane-Induced Neurodegeneration in Aged Mice.Frontiers in neuroscience · 2022Article
- [Effect of ulinastatin on isoflurane-induced neuronal apoptosis in the hippocampus of rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Neuroprotective effects of dexmedetomidine against isoflurane-induced neuronal injury via glutamate regulation in neonatal rats.Drug design, development and therapy · 2019Article
- Effects of compound 21, a non‑peptide angiotensin II type 2 receptor agonist, on general anesthesia‑induced cerebral injury in neonatal rats.Molecular medicine reports · 2018Article
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8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal exposure to isoflurane can result in neuroapoptosis and persistent cognitive impairments. However, the underlying mechanisms remain elusive. Anaphase-promoting complex/cyclosome (APC/C) and its co-activator Cdh1 are E3 ubiquitin ligases that play important roles in the central nervous system, including in the regulation of neuronal survival, synaptic development, and mammalian learning and memory. However, whether APC/C-Cdh1 is involved in isoflurane-induced neurotoxicity in developing rats remains unclear. In this study, postnatal day-7 (P7) rat pups and primary hippocampal neurons were exposed to 2% isoflurane for 6 h. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to detect neuronal apoptosis, and the expression of proteins involved in apoptosis (cleaved caspase-3, Bax and Bcl-2) was assessed by western blot. The level of Cdh1 in the hippocampus was downregulated during isoflurane-induced neuroapoptosis. Cdh1-encoding lentivirus was transfected before isoflurane-treatment to increase the level of Cdh1. Our results showed that Cdh1 overexpression by a recombinant Cdh1-encoding lentivirus reduced isoflurane-induced neuronal apoptosis. Moreover, bilateral intra-hippocampal injection with Cdh1-encoding lentivirus attenuated long-term cognitive deficits after exposure to isoflurane in developing rats. Our study indicates that Cdh1 is an important target to prevent isoflurane-induced developmental neurotoxicity.
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