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Bibenzyl compound 20c protects against endoplasmic reticulum stress in tunicamycin-treated PC12 cells in vitro
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Bibenzyl compound 20c protects against endoplasmic reticulum stress in tunicamycin-treated PC12 cells in vitro
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Bibenzyl compound 20c protects against endoplasmic reticulum stress in tunicamycin-treated PC12 cells in vitro
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Journal Article
Bibenzyl compound 20c protects against endoplasmic reticulum stress in tunicamycin-treated PC12 cells in vitro
2016
Overview
Aim： Accumulation of α-synuclein （a-syn） in the brain is a characteristic of Parkinson＇s disease （PD）. In this study, we investigated whether treatment with tunicamycin, an endoplasmic reticulum （ER） stress inducer, led to the accumulation of α-syn in PC12 cells, and where a-syn protein was accumulated, and finally, whether bibenzyl compound 20c, a novel compound isolated from Gastrodia elata （Tian ma）, could alleviate the accumulation of α-syn and ER stress activation in tunicamycin-treated PC12 cells.Methods： PC12 cells were treated with tunicamycin for different time （6 h, 12 h, 24 h, 48 h）o Cell viability was determined by a MTT assay. Subcellular fractions of ER and mitochondria were extracted with the Tissue Endoplasmic reticulum Isolation Kit. The levels of α-syn protein and ER-stress-associated downstream chaperones were detected using Western blots and immunofluorescence.Results： Treatment of PC12 cells with tunicamycin （0.5-10 pg/mL） dose-dependently increased the accumulation of a-syn monomer （19 kDa） and oligomer （55 kDa）, and decreased the cell viability. Accumulation of the two forms of a-syn was observed in both the ER and mitochondria with increasing treatment time. Co-treatment with 20c （10^5 mol/L） significantly increased the viability of tunicamycin- treated cells, reduced the level of a-syn protein and suppressed ER stress activation in the cells, evidenced by the reductions in phosphorylation of elF2a and expression of spliced ATF6 and XBPI.Conclusion： Tunicamycin treatment caused accumulation of α-syn monomer and oligomer in PC12 cells. Bibenzyl compound 20c reduces the accumulation of α-syn and inhibits the activation of ER stress, which protected PC12 cells against the toxicity induced by tunicamycin.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
