Upregulation of Cdh1 Attenuates Isoflurane-Induced Neuronal Apoptosis and Long-Term Cognitive Impairments in Developing Rats.

ABSTRACT: Neonatal exposure to isoflurane can result in neuroapoptosis and persistent cognitive impairments. However, the underlying mechanisms remain elusive. Anaphase-promoting complex/cyclosome (APC/C) and its co-activator Cdh1 are E3 ubiquitin ligases that play important roles in the central nervous system, including in the regulation of neuronal survival, synaptic development, and mammalian learning and memory. However, whether APC/C-Cdh1 is involved in isoflurane-induced neurotoxicity in developing rats remains unclear. In this study, postnatal day-7 (P7) rat pups and primary hippocampal neurons were exposed to 2% isoflurane for 6 h. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to detect neuronal apoptosis, and the expression of proteins involved in ap

SUBMITTER: Li X 

PROVIDER: S-EPMC5703863 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature