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6-OHDA mediated neurotoxicity in SH-SY5Y cellular model of Parkinson disease suppressed by pretreatment with hesperidin through activating L-type calcium channels
Authors
L. Elyasi
H.G. Hamid Abadi
+6 more
M. Jahanshahi
M. Jameie
M. Jameie
S.B. Jameie
M. Khalili
E. Nikmahzar
Publication date
1 January 2020
Publisher
Abstract
Objectives: Parkinson�s disease (PD) is a neurological condition with selective progressive degeneration of dopaminergic neurons. Routine therapies are symptomatic and palliative. Although, hesperidin (Hsd) is known for its neuroprotective effects, its exact cellular mechanism is still a mystery. Considering the important role of calcium (Ca2+) in cellular mechanisms of neurodegenerative diseases, the present study aimed to investigate the possible effects of Hsd on Ca2+ channels in cellular model of PD and the possible association between the selective vulnerability of neurons in cellular models of PD and expression of the physiological phenotype that changes Ca2+ homeostasis. Methods: SH-SY5Y cell line was used in this study; cell damage was induced by 150 µM 6-OHDA and the cells� viability was examined using MTT assay. Intracellular calcium, reactive oxygen species (ROS) and mitochondrial membrane potential were determined by the fluorescence spectrophotometry method. The expressions of calcium channel receptors were determined by gel electrophoresis and immunoblotting. Results: Loss of cell viability and mitochondrial membrane potential were confirmed in 6-OHDA treated cells. In addition, intracellular ROS and calcium levels, calcium channel receptors significantly increased in 6-OHDA-treated cells. Incubation of SH-SY5Y cells with hesperidin showed a protective effect, reduced the biochemical markers of cell damage/death, and balanced calcium hemostasis. Conclusions: Based on our findings, it seems that hesperidin could suppress the progression of the cellular model of PD via acting on intracellular calcium homeostasis. Further studies are needed to confirm the potential benefits of preventive and therapeutic effects of stabilizing cellular calcium homeostasis in neurodegenerative disease. © 2021 De Gruyter. All rights reserved
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Golestan University of Medical Sciences Repository
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oai:eprints.goums.ac.ir:10833
Last time updated on 21/11/2020
eprints Iran University of Medical Sciences
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oai:eprints.iums.ac.ir:39815
Last time updated on 18/07/2022