Endoplasmic reticulum stress pathway mediates isoflurane-induced neuroapoptosis and cognitive impairments in aged rats.

摘要: Abstract Postoperative cognitive dysfunction (POCD) is increasingly being recognized as an important clinical syndrome. Although it has been documented that volatile anesthetics induce neuronal apoptosis and deficits in several aged animal models, the underlying mechanisms are not well understood. Endoplasmic reticulum stress (ERS) considered initial or early response of cells under linked to death various neurodegenerative diseases. The study was designed explore possible role ERS pathway isoflurane-induced neuroapoptosis impairments. In present study, twenty-month-old rats were exposed 1.3% isoflurane for 4 h. Two weeks later, subjected behavioral study. Protein mRNA expressions markers evaluated. Meanwhile, hippocampal also detected. We found triggered evidenced by increased phosphorylation eukaryotic initiation factor (EIF) 2α, expression 78-kDa glucose-regulated protein (GRP78), activating transcription (ATF) 4 C/EBP homologous (CHOP). Furthermore, level hippocampus significantly up-regulated after exposure, salubrinal (ERS inhibitor) treatment attenuated increase. More importantly, impairments caused effectively alleviated pretreatment. These results indicate ERS-mediated apoptotic involved neurotoxicity rats. Inhibition overactivation contributes relief neurohistopathologic changes.