Naringin Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells

Kim, Hak-Jae; Song, Jeong Yoon; Park, Hae Jeong; Park, Hyun Kyung; Yun, Dong Hwan; Chung, Joo‐Ho

doi:10.4196/kjpp.2009.13.4.281

Cited by 84 publications

(32 citation statements)

References 27 publications

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“…6). Kim et al reported that on ROT induction, the nuclear damage was found to be high [41] which correlated with our study when ROT (20 µM) was induced in SH-SY5Y cells. Decreased nuclear damage was found during the co-treatment with SES (50 µM).…”

Section: Resultssupporting

confidence: 92%

Sesamol Antagonizes Rotenone-Induced Cell Death in Sh-Sy5y Neuronal Cells

Rohini

Krishnamurthy

2016

Int J Pharm Pharm Sci

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Objective: To investigate the neuroprotective effect of sesamol against rotenone-induced cell death in SH-SY5Y cells associated with Parkinsonism.Methods: SH-SY5Y cells were maintained in Dulbecco's modified Eagle's medium. After differentiation, the cells were incubated with rotenone (20 μM) and sesamol at different concentrations (10-100 μM). Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. The reactive oxygen species, mitochondrial membrane potential and nuclear morphology were determined by dichlorofluorescein diacetate, rhodamine 123 and 4', 6-diamidino-2-phenylindole, respectively. Thiobarbituric acid reactive substances, activities of catalase, superoxide dismutase, and glutathione peroxidase and glutathione level were determined by standard assays. Results:Sesamol significantly increased the cell viability and decreased the rotenone-induced cell death in SH-SY5Y cells. Sesamol antagonized rotenone-induced reactive oxygen species generation, loss of mitochondrial membrane potential and nuclear damage. Sesamol also decreased thiobarbituric acid reactive substances level, increased the activities of catalase, superoxide dismutase, glutathione peroxidase and increased the level of glutathione in rotenone-induced cells. Conclusion:The results obtained strongly indicate the promising neuroprotective role of sesamol against rotenone-induced death in SH-SY5Y cells.

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Section: Resultssupporting

confidence: 92%

Sesamol Antagonizes Rotenone-Induced Cell Death in Sh-Sy5y Neuronal Cells

Rohini

Krishnamurthy

2016

Int J Pharm Pharm Sci

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“…Naringin treatment decreased the apoptosis by ameliorating the expressions of Bcl-2 and Bax in cells exposed to 3-NP. Naringin has been previously reported to modulate the Bcl-2 genes and protect neurons from apoptosis [63]. Further, studies have shown that, Bcl-2 expression protects PC12 cells from 3-NP-induced mitochondrial dependent apoptosis [64].…”

Section: Discussionmentioning

confidence: 98%

Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells

Gopinath

Sudhandiran

2015

Mol Cell Biochem

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“…The signal transduction pathway leads to apoptosis, a highly organized physiological mechanism for destroying injured and abnormal cells 27,28) that may play an important role in some cellular processes of the cell cycle. Furthermore, mitochondrial cyt c releases an important control point in caspase activation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Induction of Caspase-3-Dependent Apoptosis in Human Leukemia HL-60 Cells by δ-Elemene

et al. 2011

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d-Elemene, an antitumor component, is a chemical compound isolated from Curcuma wenyujin, a Chinese traditional herb. We examined whether d-elemene could inhibit cell growth and cell cycle progression and induce apoptosis in human leukemia HL-60 cells. The results demonstrated that d-elemene induces signiˆcant apoptosis of HL-60 cells, as shown by MTT assay, annexin V (AnV) binding of externalized phosphatidylserine (PS), and the mitochondrial probe JC-1 using ‰ow cytometry. HL-60 cells treated with d-elemene showed high percentages in the early apoptotic and late apoptoctic/necrotic stages, as well as caspase-3 activation of HL-60 cells. By monitoring the changes in cell cycle proles, we conˆrmed that d-elemene could interfere with the cell cycle in the G2/M phase and induce apoptosis in HL-60 cells in a time-dependent manner. Caspase-3 plays a direct role in proteolytic cleavage of the cellular proteins responsible for progression to apoptosis. Therefore we examined apoptosis in HL-60 cells after exposure to d-elemene and measured caspase-3 activities with or without Z-Val-Ala-Asp-‰uoromethylketone (z-VAD-fmk, a broad-spectrum caspase inhibitor) pretreatment using ‰ow cytometric analysis. The results showed that d-elemene could induce caspase-3 activation as detected by the decrease in d-elemene-induced caspase-3 activities after treatment with z-VAD-fmk. In the present study, d-elemene activated typical caspase-dependent apoptosis in HL-60 cells, as demonstrated by an inhibitory eŠect of z-VAD-fmk on this cell death. During d-elemene-induced apoptosis, cytochrome c and apoptosis-inducing factor were released into the cytosol and BAX was translocated from the cytosol to mitochondria. However, these were not prevented by z-VAD-fmk. In conclusion, our study demonstrated that d-elemene could induce G2/M cell cycle transition and trigger apoptosis through a caspase-3-dependent pathway.

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Naringin Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells

Cited by 84 publications

References 27 publications

Sesamol Antagonizes Rotenone-Induced Cell Death in Sh-Sy5y Neuronal Cells

Sesamol Antagonizes Rotenone-Induced Cell Death in Sh-Sy5y Neuronal Cells

Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells

Induction of Caspase-3-Dependent Apoptosis in Human Leukemia HL-60 Cells by δ-Elemene

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