Melatonin suppresses methamphetamine-triggered endoplasmic reticulum stress in C6 cells glioma cell lines.

摘要: Methamphetamine (METH) is a neurotoxic drug that causes brain damage by inducing neuronal and glial cell death together with hyperactivity-mediated progressive neurodegeneration. Previous studies have shown METH induced hyperactivity via oxidative stress, the inflammatory response, endoplasmic reticulum stress (ER stress) mechanisms, melatonin could reverse these effects. However, exact mechanism of protective role in METH-mediated ER has not been understood. This study investigated effect against toxicity-mediated cells. Our demonstrated increased toxicity related to METH-induced stimulating unfolded protein response (UPR) activate expression transducers, including phosphorylated double-stranded RNA-activated kinase (PKR)-like (p-PERK), activating transcription factor (ATF6), inositol-requiring enzyme 1 (p-IRE1). Moreover, binding immunoglobulin (Bip), CCAAT/enhancer-binding homologous (CHOP), caspase-12, eukaryotic translation initiation 2 alpha (p-eIF2α) spliced X-box-binding protein-1 (XBP-1) mRNA were also increased. Melatonin reduced reducing genes proteins concentration-dependent manner. In addition, promoted Bip chaperone Taken together, our findings suggest can protect stress-induced METH.