Background: Propofol is an intravenous drug commonly used in anesthesia procedures
and intensive care in children. However, it also has neurotoxic effects on children. MicroRNA
plays an important role in neurological diseases and neurotoxicity.
Methods: In this study, primary rat hippocampal neurons were used to investigate the role of miR-
582-5p in propofol-induced neurotoxicity. Cell viability was monitored by 3-(4,5-dimethylthiazolyl)-
2,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while the expression
of proteins was monitored by real-time quantitation polymerase chain reaction (RT-qPCR) and
western blot. TargetScan and double luciferase report assay were used to predict the targeting relationship
between miR-582-5p and Rho-associated serine-threonine protein kinase 1 (ROCK1).
Results: In the present study, the viability of neurons and the expression of miR-582-5p were decreased
in a time-dependent manner after propofol treatment. Besides, miR-582-5p overexpression
significantly reduced the toxicity of propofol on neuron cells but had no significant effect on normal
nerve cells. In addition, miR-582-5p overexpression significantly reversed the expression of
apoptosis-related proteins (cleaved caspase 3 and cleaved caspase 9) induced by propofol but had
no significant effect in normal nerve cells. TargetScan and Dual-luciferase report assay revealed
that ROCK1 was a targeted regulatory gene for miR-582-5p, and propofol treatment up-regulated
ROCK1 expression by inhibiting miR-582-5p expression. Notably, miR-582-5p overexpression
significantly increased cell viability, while ROCK1 overexpression reversed the effect of miR-582-
Conclusion: Taken together, these findings suggest that miR-582-5p alleviated propofol-induced
apoptosis of newborn rat neurons by inhibiting ROCK1.