Prolactin prevents mitochondrial dysfunction induced by glutamate excitotoxicity in hippocampal neurons
| Autor: | N. Pavón, Lourdes Massieu, Marco Cerbón, Erika Alejandra Cabrera-Reyes, Teresa Montiel, Ma. I. Coronado-Mares, Nadia Alejandra Rivero-Segura, I. Pérez-Torres, Ruth Rincon-Heredia |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
endocrine system medicine.medical_specialty Primary Cell Culture Excitotoxicity Glutamic Acid Mitochondrion Hippocampal formation medicine.disease_cause Hippocampus Neuroprotection Antioxidants Lipid peroxidation 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Malondialdehyde Internal medicine Autophagy medicine Animals Rats Wistar Superoxide Dismutase General Neuroscience Glutamate receptor Prolactin Mitochondria Rats Neuroprotective Agents 030104 developmental biology Endocrinology chemistry Hypothalamus Lipid Peroxidation hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery |
| Zdroj: | Neuroscience Letters. 701:58-64 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/j.neulet.2019.02.027 |
| Popis: | Prolactin (PRL) is a pleiotropic hormone secreted by several cells and tissues in the body, such as mammary glands, T-lymphocytes, hypothalamus, among others. This hormone possess neuroprotective properties against glutamate-excitotoxicity through the activation of NF-kB, suggesting it could exert an antioxidant action. However, the role of PRL on the antioxidant defense during glutamate-induced excitotoxicity is not clear to date. Therefore, in the present study, we have evaluated the effect of PRL on SOD activity and protein content of both of its isoforms (Mn2+-SOD and Cu2+/Zn2+-SOD), as well as, its action on mitochondrial activity in primary culture of hippocampal neurons of rats. Additionally, we have evaluated the possible antioxidant effect of PRL through the determination of lipid peroxidation products (LPO), measured as malondialdehyde (MDA). Results show that PRL enhances the activity and the protein content of Mn2+-SOD and Cu2+/Zn2+-SOD in neurons exposed to glutamate-induced excitotoxicity. Moreover, our results demonstrate that PRL prevents mitochondrial dysfunction induced by glutamate and significantly decreases the levels of LPO products. To our knowledge, this is the first time that a potential antioxidant effect of PRL has been described in hippocampal neurons exposed to glutamate excitotoxicity, opening questions of its potentiality for therapeutics. |
| Databáze: | OpenAIRE |
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