ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2024
The duration-dependent and sex-specific effects of neonatal sevoflurane exposure on cognitive function in rats.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The NLRP3 Inflammasome: A Central Mediator in Sevoflurane-Induced Neurotoxicity and A Potential Target for Neuroprotection.Molecular neurobiology · 2026Review
- Mechanisms of natural compounds in treating inhalation anesthesia-induced cognitive dysfunction.Frontiers in pharmacology · 2026Review
- Estrogen Alleviates Sevoflurane-Induced Neurotoxicity by Inhibiting ERα-Tau Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neonatal Sevoflurane Exposure Exerts Sex-Specific Effects on Cognitive Function via C3- and TLR4-Related M1/M2 Microglial Cell Polarisation in Rats.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
7 authors.
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Abstract
Clinical studies have found that neonatal sevoflurane exposure can increase the risk of cognitive dysfunction. However, recent studies have found that it can exhibit neuroprotective effects in some situations. In this study, we aimed to explore the effects of sevoflurane neonatal exposure in rats. A total of 144 rat pups (72 males and 72 females) were assigned to six groups and separately according to sevoflurane exposure of different times on the seventh day after birth. Blood gas analysis and western blot detection in the hippocampus were conducted after exposure. The Morris water maze test was conducted on the 32nd to 38th days after birth. The expression of PSD95 and synaptophysin in the hippocampus was detected after the Morris water maze test. We found that neonatal exposure to sevoflurane promoted apoptosis in the hippocampus, and Bax and caspase-3 were increased in a dose-dependent manner. The 2-h exposure had the greatest effects on cognitive dysfunction. However, with the extension of exposure time to 6 h, the effects on cognitive function were partly compensated. In addition, sevoflurane exposure decreased synaptogenesis in the hippocampus. However, as the exposure time was extended, the suppression of synaptogenesis was attenuated. In conclusion, neonatal sevoflurane exposure exhibited duration-dependent effects on cognitive function via Bax-caspase-3-dependent apoptosis and bidirectional effects on synaptogenesis in rats.
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