Repository of Research and Investigative Information

Repository of Research and Investigative Information

Baqiyatallah University of Medical Sciences

Neuroprotective and Antiapoptotic Effects of Allopregnanolone and Curcumin on Arsenic-Induced Toxicity in SH-SY5Y Dopaminergic Human Neuroblastoma Cells

(2020) Neuroprotective and Antiapoptotic Effects of Allopregnanolone and Curcumin on Arsenic-Induced Toxicity in SH-SY5Y Dopaminergic Human Neuroblastoma Cells. Neurophysiology. pp. 124-133. ISSN 0090-2977

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Neuroprotective and Antiapoptotic Effects of Allopregnanolone and Curcumin on Arsenic-Induced Toxicity in SH-SY5Y Dopaminergic Human Neuroblastoma Cells.pdf

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Abstract

Parkinson's disease (PD) is a widespread neurological disorder mainly characterized by gradual death of dopaminergic neurons in the basal ganglia. In our study, we compared the effects of curcumin (Curc) as a herbal medicine and those of allopregnanolone (Allo) as a synthetic drug on arsenic(Ars-)-induced toxicity in an SH-SY5Yin vitromodel of PD. Cell survival was determined by the MTT assay; intracellular reactive oxygen species (ROSs) and the mitochondrial potential were assessed by a fluorescence probe. Furthermore, immunoblotting was applied to determine the biomarkers of cells apoptosis. As was found, Ars decreases the cell survival rate and enhances the loss of the mitochondrial membrane potential. The mean contents of intracellular ROSs, amount of c-Fos, and caspase-3 ratio significantly increased in Ars-exposed cells. Pretreatment of cells with Allo (250 mu M) and Curc (5 mu M) significantly decreased mean levels of these factors in Ars-treated cells. Although Curc showed a greater protective effect than Allo, the respective difference was statistically insignificant. The neuroprotective effects of Allo and Curc are probably related to their antioxidant and anti-apoptotic properties, which suggests their therapeutic potential in PD treatment.

Item Type: Article
Keywords: Parkinson's disease arsenic SH-SY5Y cells allopregnanolone curcumin apoptosis oxidative stress mitochondrial dysfunction induced neurotoxicity parkinsons-disease rat model c-fos mechanisms apoptosis neurosteroids activation Neurosciences & Neurology Physiology
Page Range: pp. 124-133
Journal or Publication Title: Neurophysiology
Journal Index: ISI
Volume: 52
Number: 2
Identification Number: https://doi.org/10.1007/s11062-020-09861-6
ISSN: 0090-2977
Depositing User: مهندس مهدی شریفی
URI: http://eprints.bmsu.ac.ir/id/eprint/8547

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