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It is well established that exposure of common anesthetic isoflurane in early life can induce neuronal apoptosis and long-lasting cognitive deficit, but the underlying mechanisms were not well understood. The cell cycle protein Cyclin B1 plays an important role in the survival of postmitotic neurons. In the present study, we investigated whether cyclin B1-mediated cell cycle activation pathway is a contributing factor in developmental isoflurane neurotoxicity.

Early life exposure to general anesthetics can have neurotoxic consequences. Evidence indicates that xenon, a rare noble gas with anesthetic properties, may lessen neuronal damage under certain conditions. However, its potential neuroprotective properties, when used alone or in combination with other anesthetics, remain largely unknown. While it is difficult to verify the adverse effects of long duration anesthetic exposure in infants and children, the utilization of relevant non-clinical models (i.e., human-derived neural stem cells) may serve as a “bridging” model for evaluating the vulnerability of the nervous system.

Animal studies have shown that early postnatal propofol administration is involved in neurobehavioral alterations in adults. However, the underlying mechanism is not clear.

Evidence has shown that propofol may cause widespread apoptotic neurodegeneration. Hypoxic preconditioning has been demonstrated to provide neuroprotection and brain recovery from both acute and chronic neurodegeneration in several cellular and animal models. However, the mechanism has not been well elucidated. Therefore, the present study was designed to investigate the expression of glucose transporters (GLUT1 and GLUT3) and mitochondrial division and fusion (Drp1 and Mfn2) proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity.

Excessive exposure to commonly used anesthetic agents, such as ketamine, may induce permanent damage to immature human brains. In this work, we used a human embryonic stem cell (hESC)-derived neuron model to assess the expression and function of human microRNA 735 (hsa-miR-375) in regulating ketamine-induced neural cell death and neural toxicity in vitro. In the in vitro culture, hESC-derived neurons were incubated with ketamine for 72 h. After that, cell viability, reactive oxygen species activity, neural apoptosis, neurite degeneration, and hsa-miR-375 gene expression were assessed, respectively.

Most clinically used general anesthetics have demonstrated neurotoxicity in animal studies, but the related mechanisms remain unknown. Previous studies suggest that anesthetics affect neuronal development through neuroinflammation, and significant effects of neuroinflammation on neurogenesis and neuronal disease have been shown. In the present study, we treated pregnant mice with 2% sevoflurane for 3 h at gestational day 15.5 and analyzed the expression of proinflammatory cytokines, including IL-6 and IL-17, in fetal mice brains. Sevoflurane induced IL-6 mRNA significantly, but did not upregulate IL-17.