DL-3-n-butylphthalide promotes dendrite development in cortical neurons subjected to oxygen-glucose deprivation/reperfusion.

The limited degree of functional recovery is closely associated with the condition of the periinfarct cortex after ischemic stroke. The model of oxygen-glucose deprivation in cultured neurons could partly simulate this condition. Proper dendritic morphology is crucial for the correct wiring of neuronal function. Hence, the question of how to facilitate the plasticity of neural dendrites is of great significance. DL-3-n-butylphthalide is an efficient medication for ischemic stroke. In this study, in addition to having neuroprotective effects, DL-3-n-butylphthalide could increase the number of primary and secondary dendrites and of dendritic tips as confirmed by Sholl analysis. This study further demonstrated that DL-NBP inactivates PI3K/AKT signaling to positively regulate dendritic branching.