Propofol inhibited autophagy through Ca²⁺/CaMKKβ/AMPK/mTOR pathway in OGD/R-induced neuron injury.

ABSTRACT:

Background

The neuroprotective role of propofol (PPF) in cerebral ischemia-reperfusion (I/R) has recently been highlighted. This study aimed to explore whether the neuroprotective mechanisms of PPF were linked to its regulation of Ca²⁺/CaMKKβ (calmodulin-dependent protein kinase kinase β)/AMPK (AMP-activated protein kinase)/mTOR (mammalian target of rapamycin)/autophagy pathway.

Methods

Cultured primary rat cerebral cortical neurons were treated with oxygen-glucose deprivation and re-oxygenation (OGD/R) to mimic cerebral I/R injury in vitro.

Results

Compared with the control neurons, OGD/R exposure successfully induced neuronal I/R injury. Furthermore, OGD/R exposure notably caused autophagy induction, reflected by augmented LC3-II/LC3-I ratio and Beclin 1

SUBMITTER: Sun B 

PROVIDER: S-EPMC6251140 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature