@article{APS3535,
author = {Jin-feng BAO and Ren-gang WU and Xiao-ping ZHANG and Yan SONG and Chang-ling LI},
title = {Melatonin attenuates 1-methyl-4-phenylpyridinium-induced PC12 cell death},
journal = {Acta Pharmacologica Sinica},
volume = {26},
number = {1},
year = {2016},
keywords = {},
abstract = {Aim:To explore the effect of melatonin on PC12 cell death induced by 1-methyl-
4-phenylpyridinium (MPP+).
Methods: MTT assay, lactate dehydrogenase (LDH)
efflux assay, and immunohistochemistry methods were used to measure neurotoxicity
of PC12 cells treated acutely with MPP+ in low glucose and high glucose
conditions, and to assess the neuroprotective effect of melatonin on PC12 cell
death induced by MPP+.
Results: In a low glucose condition, MPP+ significantly
induced PC12 cell death, which showed time and concentration dependence. In a
serum-free low glucose condition, the percentages of viability of cells treated
with MPP+ for 12, 24, 48, 72, and 96 h were 85.1%, 75.4%, 64.9%, 28.15%, and
9%, respectively. The level of LDH in the culture medium increased and tyrosine
hydroxylase positive (TH+) cell count decreased. However, in a serum-free high
glucose condition, MPP+ did not significantly induce PC12 cell death compared
with control at various concentrations and time regimens. When the cells were
preincubated with melatonin 250 μmol/L for 48, 72, and 96 h in a serum-free low
glucose condition, cell survival rate significantly increased to 78.1%, 58.8%, and
31.6%, respectively. Melatonin abolished the LDH leakage of cells treated with
MPP+ and increased TH+ cells count.
Conclusion: MPP+ caused concentrationdependent
PC12 cell death. The level of glucose was an important factor to MPP+
induced dopaminergic PC12 cell death. Low glucose level could potentiate MPP+
toxicity, while high glucose level could reduce the toxicity. In addition, melatonin
attenuated PC12 cell death induced by MPP+.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/3535}
}