Objective: Early exposure to general anesthesia in children might be a potentially highrisk
factor for learning and behavioral disorders. The mechanism of neurotoxicity induced by general
anesthesia was not defined. miR-496 could regulate cerebral injury, while the roles of miR-
496 in neurotoxicity were not elucidated. Therefore, we aimed to investigate the effects of miR-
496 in neurotoxicity induced by propofol.
Methods: Primary Prefrontal Cortical (PFC) neurons were isolated from neonatal rats and treated
with propofol to induce neurotoxicity. Cell viability was detected by (3-(4,5-Dimethylthiazol-
2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell apoptosis was assessed by terminal
deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The target relationship of
miR-496 and Rho Associated Coiled-Coil Containing Protein Kinase 2 (ROCK2) was explored
using luciferase assays.
Results: Propofol decreased cell viability, promoted cell apoptosis, and decreased the expression
of miR-496 in PFC neurons in a dose-dependent manner. Overexpression of miR-496 attenuated
neurotoxicity induced by propofol in PFC neurons. ROCK2 was a target of miR-496, and miR-496
oppositely modulated the expression of ROCK2. Besides, propofol increased the expression of
ROCK2 through inhibiting miR-496 in PFC neurons. Overexpression of miR-496 attenuated propofol-
induced neurotoxicity by targeting ROCK2 in PFC neurons.
Conclusion: miR-496 was decreased in PFC neurons treated with propofol, and overexpression of
miR-496 attenuated propofol-induced neurotoxicity by targeting ROCK2. miR-496 and ROCK2
may be promising targets for protecting propofol-induced neurotoxicity.