Publication: Melatonin prevents calcineurin-activated the nuclear translocation of nuclear factor of activated T-cells in human neuroblastoma SH-SY5Y cells undergoing hydrogen peroxide-induced cell death
Issued Date
2020-07-01
Resource Type
ISSN
18736300
08910618
08910618
Other identifier(s)
2-s2.0-85084368292
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Chemical Neuroanatomy. Vol.106, (2020)
Suggested Citation
Asawin Premratanachai, Wilasinee Suwanjang, Piyarat Govitrapong, Jirapa Chetsawang, Banthit Chetsawang Melatonin prevents calcineurin-activated the nuclear translocation of nuclear factor of activated T-cells in human neuroblastoma SH-SY5Y cells undergoing hydrogen peroxide-induced cell death. Journal of Chemical Neuroanatomy. Vol.106, (2020). doi:10.1016/j.jchemneu.2020.101793 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/56336
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Title
Melatonin prevents calcineurin-activated the nuclear translocation of nuclear factor of activated T-cells in human neuroblastoma SH-SY5Y cells undergoing hydrogen peroxide-induced cell death
Abstract
© 2020 Elsevier B.V. The interaction between the activation of protein phosphatase, calcineurin (CaN), and the dephosphorylation and nuclear translocation of nuclear factor of activated T-cells (NFAT), a transcriptional factor in the immune system, has attracted interest as a key factor responsible for the cell death process. In this study, the effects of melatonin on the interaction between CaN and NFAT signaling during oxidative stress-induced cell death were investigated. Human neuroblastoma SH-SY5Y cells were treated with the non-radical reactive oxygen species hydrogen peroxide (H2O2). Cells were treated with 200 μM H2O2 for the indicated time. Some H2O2-treated cells were pretreated with melatonin for 1 h. Control cells were treated with the same concentration of ethanol used to dilute melatonin. H2O2-induced cell death promoted increases in reactive oxygen species (ROS) production and the nuclear translocation of NFAT, which were related to increased levels the active, cleaved form of CaN (32.5 kDa). In addition, pretreatment of H2O2-treated cells with melatonin decreased cell death, ROS production, the levels of the active-cleaved form of CaN and the nuclear translocation of NFAT. Based on these findings, melatonin may exert its neuroprotective effects on oxidative damage-induced cell death by inhibiting CaN-activated the nuclear translocation of NFAT.