Silibinin exerts neuroprotective effects against cerebral hypoxia/ reoxygenation injury by activating the GAS6/Axl pathway

Ischemic stroke is regarded one of the most common causes of brain vulnerability. Silibinin (SIL), extracted from the seeds of Silybinisus laborinum L., has been found to exhibit obvious therapeutic effects on neurodegenerative diseases. GAS6 has been proven to have significant neuroprotective effects; however, the role of SIL and GAS6 in ischemic stroke remains unclear. This study aimed to investigate the protective effects of SIL against cerebral ischemia-reperfusion injury in neuroblastoma N2a cells, as well as the mechanisms involved. Firstly, the toxicity of SIL was evaluated, and safe concentrations were chosen for subsequent experiments. Then, SIL exerts significant neuroprotection against hypoxia/reoxygenation (HR) injury in N2a cells, as manifested by increased cell viability, decreased apoptotic rate, LDH, and ROS generation. Additionally, SIL was found to inhibit HR-induced apoptosis, mitochondria dysfunction, and oxidative stress. However, silencing of GAS6 inhibited the neuro protective effects of SIL. To sum up, these results suggest that SIL may be a promising therapeutic agent for the treatment of ischemic stroke.

Automated summary

This study aimed to investigate the protective effects of silibinin against cerebral ischemia-reperfusion injury in neuroblastoma N2a cells, as well as the mechanisms involved. The results showed that silibinin significantly reduced cell death, apoptotic rate, LDH, and ROS generation, and inhibited mitochondrial dysfunction and oxidative stress. However, the protective effects of silibinin were weakened when GAS6 was silenced.