Ghrelin protects MES23.5 cells against rotenone via inhibiting mitochondrial dysfunction and apoptosis |
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| Institution: | 1. Department of Clinical Pharmacology, Faculty of Medicine, Alexandria University, Alexandria, Egypt;2. Department of Histology and cell Biology, Faculty of Medicine, Alexandria University, Alexandria, Egypt;1. Molecular Neurophysiology, Department of Neuroscience Research, National Institute of Psychiatry Ramón de la Fuente Muñiz (INPRFM), México;2. School of Dietetics and Nutrition, ISSSTE, Callejón Vía San Fernando 12, México City, Mexico;3. Department of Neurochemistry and Neuropharmachology, Institut d''Investigacions, Biomèdiques de Barcelona, CSIC-IDIBAPS, CIBERNED, c/Rosselló 161, 6a, E-08036 Barcelona, Spain;1. Department of orthopedics, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China;2. Department of Orthopedics, Shanghai Changzheng Hospital, 200000 Shanghai, China;3. Department of Neurology, Nantong Second People''s Hospital, Nantong 226001, Jiangsu Province, China;4. Department of Orthopedic Surgery, Shanghai Jiaotong University Affiliated Sixth People''s Hospital, 200233 Shanghai, China;5. Department of Medical image, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China;1. National Institute of Science and Technology in Nanobiopharmaceutics (INCT — Nanobiofar), Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil;2. Institute of Cardiology, University Foundation of Cardiology, Porto Alegre, Rio Grande do Sul, Brazil;3. Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Münster, Germany;1. Laura Bassi Centre of Expertise THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, Paracelsus Medical University, Müllner Hauptstraße 48, 5020 Salzburg, Austria;2. Department of Cell Biology, University of Salzburg, Hellbrunnerstraße 34, 5020 Salzburg, Austria;3. Institute of Physiology and Pathophysiology, Paracelsus Medical University, Strubergasse 21, 5020 Salzburg, Austria;4. Gastein Research Institute, Paracelsus Medical University, Strubergasse 21, 5020 Salzburg, Austria;5. Division of Molecular Dermatology, Department of Dermatology, Paracelsus Medical University, Müllner Hauptstraße 48, 5020 Salzburg, Austria;6. Procomcure Biotech GmbH, Austria |
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| Abstract: | Ghrelin is an endogenous ligand for the growth hormone secretagogue (GHS) receptor and has several important physiological functions. Recently, particular attention has been paid to its neuroprotective effect. Rotenone is used to investigate the pathogenesis of Parkinson's disease (PD) for its ability to inhibit mitochondrial complex I. The current study was carried out to investigate the neuroprotective effects of ghrelin against rotenone in MES 23.5 dopaminergic cells and explored the possible mechanisms underlying this protection. Our results showed that rotenone induced significant decrease in cell viability which was counteracted by ghrelin treatment. In addition, rotenone challenge reduced mitochondrial membrane potential, inhibited the activity of mitochondrial complex I and depressed cytochrome C release from mitochondria. This mitochondrial dysfunction was reversed by ghrelin treatment. Furthermore, our results demonstrated that ghrelin protected MES23.5 cells against rotenone-induced apoptosis by inhibiting activation of caspase-3. Overall, our findings showed ghrelin provided protective effects on MES23.5 dopaminergic cells against rotenone via restoring mitochondrial dysfunction and inhibiting mitochondrial dependent apoptosis. |
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