The Investigation of the Induction of Diketocarotenoids Senescence in SHSY-5Y Cells

Report of Health Care

مقاله 5، دوره 5، شماره 1، فروردین 2019، صفحه 37-44   

نوع مقاله: Original Article

نویسندگان

Zahra Zare Dorahi¹؛ Mojtaba Ilani²؛ Mohabbat Jamhiri³؛ Afrooz Daneshparvar¹؛ Shahrokh Zare¹؛ Meysam Zare⁴؛ Iman Jamhiri^{* 1}

¹Stem Cell Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

²Department of Physiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.

³Department of Medical Physiology, Faculty of Medicine Shahid Sadoughi University of Medical Sciences, Yazd, Iran

⁴Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

تاریخ دریافت: 12 اسفند 1396،  تاریخ بازنگری: 09 مهر 1397،  تاریخ پذیرش: 14 مهر 1397 

چکیده

Introduction: Recently, studies of diketocarotenoids such as astaxanthin (Ax) and canthaxanthin (Cx) with powerful antioxidant have focused on numerous biological mechanisms such as singlet oxygen quenching, radical scavenging, anti-diabetic, anti-carcinogenesis, anti-inflammatory, anti-obesity and anti-melanogenesis activities. There is evidence demonstrating that diketocarotenoid confers neuroprotective effects in experimental models of chronic neurodegenerative disorders and neurological diseases. This study used Ax and Cx to detect its role on senescence of SHSY-5Y Cells. Methods: In this study, the sample included the cell control group (SH-SY5Y cell line) that did not receive Ax and Cx, , and the experimental group that received Ax and Cx (20 mM). Ax and Cx were treated with SH-SY5Y cell line at 48 hours. To measure the expression of BAX, Bcl-2 and PPARγ different groups were compared by real‑time PCR analysis. The cell senescence effects of Ax and Cx, a β-galactosidase (SA-β-gal) senescence assay was evaluated. The results were analyzed by the one-way analysis of variance (ANOVA) using Prism version 6.0 software. Results: The results showed that treatment with Ax and Cx (20 mM) for 48h induced apoptosis and senescence. The BAX and Bcl-2 gene expression analysis revealed a significant impact of Ax and Cx in apoptosis induction (P<0.05). The measuring of cell senescence also indicated that Ax and Cx exhibited a senescence inductive activity as determined by an increase in β-galactosidase activity and PPARγ gene expression (P<0.05). Conclusion: It appears that Ax and Cx have therapeutic properties in SH-SY5Y cells and can cause the proliferation of these cells to cease. The results suggest that Ax and Cx treatment may be beneficial for therapy of neuroblastoma and neurodegenerative disorders.

کلیدواژه‌ها

Astaxanthin؛ Canthaxanthin؛ Apoptosis؛ Senescence؛ Neuroblastoma؛ SHSY-5Y Cells

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