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LanCL1 protects developing neurons from long-term isoflurane anesthesia-induced neurotoxicity

神经毒性 异氟醚 麻醉 期限(时间) 医学 神经科学 毒性 心理学 内科学 物理 量子力学
作者
Wenjia Xie,Yuqing Xi,Daoqian Dong,Shuai Liu,Zhengliang Ma,Liangyu Peng,Tianjiao Xia,Xiaoping Gu
出处
期刊:Experimental Neurology [Elsevier BV]
卷期号:381: 114880-114880 被引量:2
标识
DOI:10.1016/j.expneurol.2024.114880
摘要

Research has revealed that prolonged or repeated exposure to isoflurane, a common general anesthetic, can lead to cognitive and behavioral deficiencies, particularly in early life. The brain contains a wealth of LanCL1, an antioxidant enzyme that is thought to mitigate oxidative stress. Nevertheless, its precise function in mammals remains uncertain. This study uncovered a decrease in the expression of LanCL1 due to prolonged isoflurane anesthesia, accompanied by anesthesia-induced neurotoxicity in vivo and in vitro. To better understand LanCL1's essential function, LanCL1 overexpressing adenoviruses were employed to increase LanCL1 levels. The outcomes were analyzed using western blot and immunofluorescence methods. According to the findings, extended exposure to isoflurane anesthesia may lead to developmental neurotoxicity in vivo and in vitro. The anesthesia-induced neurotoxicity was concomitant with a reduction in LanCL1 expression. Moreover, the study revealed that overexpression of LanCL1 can mitigate the neurotoxic effects of isoflurane anesthesia, resulting in improved synaptic growth, less reactive oxygen species enhanced cell viability and rescued memory deficits in the developing brain. In conclusion, prolonged anesthesia-induced LanCL1 deficiency could be responsible for neurotoxicity and subsequent cognitive impairments in the developing brain. Additional LanCL1 counteracts this neurotoxic effect and protects neurons from long-term isoflurane anesthesia.
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