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. 2018 Mar 30;42(1):182–192. doi: 10.3892/ijmm.2018.3607

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Copyright: © Lin et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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The mechanisms of melatonin protected neurons against ER-induced apoptosis after cerebral ischemia. Melatonin not only attenuated the phosphorylation of PRKR-like endoplasmic reticulum kinase (PERK) and eukaryotic translation initiation factor 2α (p-eIF2α) but also reduced the expression of activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP). At the same time, cytochrome c (Cyto c) was restrained and the expression of caspase-3 was reduced. These results suggest that attenuation of ER stress-induced apoptosis is due to the mechanisms of melatonin.