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Oxytocin Alleviates MPTP-Induced Neurotoxicity in Mice by Targeting MicroRNA-26a/Death-Associated Protein Kinase 1
Hasan A M M Almansoub1,2,3, Hui Tang1,2, Ying Wu1,2
1Department of Pathophysiology, Key lab of a neurological disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Abstract:
Neurotoxicity is one of the major pathological changes in multiple neurological disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD), the second popular neurodegenerative disease in aged people. It is known that the AD and PD share the similar neuropathological hallmarks, such as the oxidative stress, loss of specific neurons, and aggregation of specific proteins. However, there are no effective therapeutic drugs for both AD and PD yet. Oxytocin (OXT) is a small peptide with 9 amino acids that is neuroprotective to many neurological disorders. Whether OXT administration confers neuroprotection to 1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP)-induced neurotoxicity in mice are still not known. In this study, we first found that the OXT levels are decreased in MPTP mice. Supplementation with OXT effectively rescues the locomotor disabilities and anxiety-like behaviors in MPTP mice. OXT also alleviates the hyperphosphorylation of α-synuclein at S129 site and the loss of dopaminergic neurons in the substantia nigra pars compacta, as well as the oxidative stress in the MPTP mice, and alleviates both oxidative stress and cell cytotoxicity in vitro. Furthermore, we found that OXT could inhibit the miR-26a/DAPK1 signal pathway in MPTP mice. In summary, our study demonstrates protective effects of OXT in MPTP mice and that miR-26a/DAPK1 signaling pathway may play an important role in mediating the protection of OXT.
Insights
Oxytocin (OXT) protects against neurotoxicity in a mouse model of Parkinson's disease by reducing oxidative stress and neuronal loss. This study reveals OXT's therapeutic potential for neurodegenerative disorders.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Neurotoxicity is a key feature of neurodegenerative diseases like Alzheimer's and Parkinson's.
- Current treatments for these conditions are limited, highlighting the need for novel therapeutic strategies.
- Oxytocin (OXT), a neuroprotective peptide, is being investigated for its potential in neurological disorders.
Purpose of the Study:
- To investigate the neuroprotective effects of Oxytocin (OXT) in a mouse model of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced neurotoxicity.
- To explore the underlying mechanisms of OXT's protective action, including its impact on oxidative stress, neuronal loss, and specific signaling pathways.
Main Methods:
- MPTP was used to induce neurotoxicity in mice, and OXT levels were measured.
- Behavioral tests were conducted to assess locomotor function and anxiety-like behaviors.
- Histological analysis examined dopaminergic neuron loss and α-synuclein hyperphosphorylation.
- In vitro assays evaluated OXT's effects on oxidative stress and cell cytotoxicity.
- The miR-26a/DAPK1 signaling pathway was investigated in MPTP-treated mice.
Main Results:
- OXT levels were found to be decreased in MPTP-induced neurotoxic mice.
- OXT administration improved locomotor function and reduced anxiety-like behaviors.
- OXT alleviated dopaminergic neuron loss and α-synuclein hyperphosphorylation in the substantia nigra.
- OXT demonstrated protective effects against oxidative stress and cytotoxicity in vitro.
- OXT was found to inhibit the miR-26a/DAPK1 signaling pathway in MPTP mice.
Conclusions:
- Oxytocin (OXT) exhibits significant neuroprotective effects in a mouse model of Parkinson's disease.
- OXT mitigates motor deficits, anxiety, dopaminergic neurodegeneration, and oxidative stress.
- The miR-26a/DAPK1 signaling pathway is implicated in mediating OXT's neuroprotective actions.
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