α-Lipoic acid inhibits sevoflurane-induced neuronal apoptosis through PI3K/Akt signalling pathway

Cell Biochemistry and Function
Rong MaZhengnian Ding

Abstract

Sevoflurane is a widely used anaesthetic agent, including in anaesthesia of children and infants. Recent studies indicated that the general anaesthesia might cause the cell apoptosis in the brain. This issue raises the concerns about the neuronal toxicity induced by the application of anaesthetic agents, especially in the infants and young children. In this study, we used Morris water maze, western blotting and immunohistochemistry to elucidate the role of α-lipoic acid in the inhibition of neuronal apoptosis. We found that sevoflurane led to the long-term cognitive impairment in the young rats. This adverse effect may be caused by the neuronal death in the hippocampal region, mediated through PI3K/Akt signalling pathway. We also showed that α-lipoic acid offset the effect of sevoflurane on the neuronal apoptosis and cognitive dysfunction. This study elucidated the potential clinical role of α-lipoic acid, providing a promising way in the prevention and treatment of long-term cognitive impairment induced by sevoflurane general anesthesia.

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Citations

Jan 10, 2018·Frontiers in Pharmacology·Patrícia Molz, Nadja Schröder
Dec 19, 2017·Frontiers in Neuroscience·Anastasia V ShindyapinaYuri L Dorokhov
Aug 27, 2016·Journal of Neurosurgical Anesthesiology·Richard J LevyFrancis X McGowan
Mar 21, 2019·Current Opinion in Anaesthesiology·Vanessa Marchesini, Nicola Disma
Aug 22, 2018·Journal of Anesthesia·Li-Jun BoZhen-Ming Dong
Dec 30, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Lubin HuangHong Ning

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AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis