Dataset Information

Oxytocin Attenuates Methamphetamine-Induced Apoptosis via Oxytocin Receptor in Rat Hippocampal Neurons.

ABSTRACT: Methamphetamine (METH) is a highly neurotoxic psychoactive substance that can directly damage the central nervous system through prolonged use. Oxytocin (OT) has attracted much attention because of its neuroprotective effect. The purpose of this study was to investigate whether OT is neuroprotective against METH-induced damage in rat hippocampal neurons. Our results revealed that pre-incubation with OT significantly prevented the damage of METH to hippocampal neurons, including the decrease of mitochondrial membrane potential and the increase of ROS (reactive oxygen species). OT pre-incubation attenuated the up-regulation of Cleaved-Caspase-3 expression and the down-regulation of Bcl-2/Bax expression induced by METH. Pre-incubation with OT prevented the decrease in oxytocin receptor density and P-CREB (phosphorylation of cAMP-response element binding) expression induced by METH in rat hippocampal neurons. Moreover, Pre-incubation of atosiban (ATO) significantly prevented these changes. In conclusion, our study proved that pre-administration of OT could significantly attenuate hippocampal neuron apoptosis induced by METH. Oxytocin receptor activation is involved in the preventive effect of OT on METH-induced apoptosis in rat hippocampal neurons.

SUBMITTER: Li C

PROVIDER: S-EPMC8415150 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Oxytocin Attenuates Methamphetamine-Induced Apoptosis <i>via</i> Oxytocin Receptor in Rat Hippocampal Neurons.

Li Chunli C Wang Haipeng H Wang Min M Chen Chunyun C Bai Fei F Ban Mengqi M Wu Chunfu C

Frontiers in pharmacology 20210812

Methamphetamine (METH) is a highly neurotoxic psychoactive substance that can directly damage the central nervous system through prolonged use. Oxytocin (OT) has attracted much attention because of its neuroprotective effect. The purpose of this study was to investigate whether OT is neuroprotective against METH-induced damage in rat hippocampal neurons. Our results revealed that pre-incubation with OT significantly prevented the damage of METH to hippocampal neurons, including the decrease of m ...[more]

PMID: 34483895

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Project description:BackgroundPropofol is a commonly used general anesthetic that may cause neuronal damage, especially in infants and young children. Mitochondria play an essential role in cellular metabolism and signal transduction. Propofol may cause neurotoxicity by inhibiting mitochondrial function, but the mechanism by this which occurs remains unclear.MethodsFirst, the primary rat hippocampal neurons were cultured for 7 days in vitro. The neurons were incubated with propofol at different times or different concentrations, and then the adenosine triphosphate (ATP), reactive oxygen species (ROS), mitochondrial membrane potential, and apoptosis-related proteins were analyzed. Based on the results of the 1st phase, the neurons were then incubated with propofol (100 µM) or corresponding reagents, including 5-aminoimidazole-4-carboxamide ribonucleotide, tenovin-1, and pifithrin-α. Subsequently, the ATP, ROS, mitochondrial membrane potential, phospho-adenosine 5'-monophosphate-activated protein kinase (p-AMPK), protein 53 (p53), and related apoptosis proteins were analyzed.ResultsHigher propofol concentrations or longer incubation times were associated with more pronounced decreases in ATP, B-cell lymphoma 2 (Bcl-2), and mitochondrial membrane potential, and more pronounced increases in ROS, BCL2-associated X (Bax), Cytochrome C (CytC), and cleaved caspase-9. Additionally, after incubation with propofol (100 µM), neuronal Bcl-2, p-AMPK, ATP, and mitochondrial membrane potential were downregulated, and ROS, p53, CytC, Bax, cleaved caspase-3, and cleaved caspase-9 were upregulated. AMPK activators or p53 inhibitors reversed the above-mentioned changes.ConclusionsPropofol (100 µM)-induced mitochondrial damage in fetal rat hippocampal neurons may be mediated by the AMPK/p53 signaling pathway. Propofol (100 µM) was shown to inhibit the activity of AMPK in neurons, upregulate the expression of p53, and then activate the mitochondrial-dependent apoptosis pathway, which may lead to neuronal apoptosis.

Dataset Information

Oxytocin Attenuates Methamphetamine-Induced Apoptosis via Oxytocin Receptor in Rat Hippocampal Neurons.

Publications

Oxytocin Attenuates Methamphetamine-Induced Apoptosis <i>via</i> Oxytocin Receptor in Rat Hippocampal Neurons.

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