Reverse relationship between autophagy and apoptosis in an in vitro model of cortical neuronal injury.

Autophagy and apoptosis are intertwined, and their relationship involves complex cross-talk. Whether the activation and inhibition of autophagy protect or damage neurons in the central nervous system has been a matter of longstanding controversy. We investigated the effect of autophagy on the apoptosis of cortical neurons after oxygen- and glucose-deprivation/reoxygenation (OGD/R) injury in vitro and found that protective mechanism activation was the predominant response to enhanced autophagy activation and increased autophagic flux.

Neuritin attenuates oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury by promoting autophagic flux.

The autophagy/apoptosis interaction has always been a focus of study in pathogenicity models. Neuritin is a neurotrophic factor that is highly expressed primarily in the central nervous system. Our previous study revealed that it protects against apoptosis in cortical neurons subjected to oxygen-glucose deprivation (OGD)/reoxygenation (OGD/R), and later animal experiments revealed that it can increase the expression of the autophagy-related protein LC3.