Fig. 4.

A schematic model illustrates the anti-oxidative and anti-inflammatory effects of edaravone in response to H₂O₂-mediated oxidative stress or LPS-induced neurotoxic inflammatory insults. In astrocyte, H₂O₂-introduced oxidative stress induced the inhibition of Akt and Bcl-2 and activated apoptosis promoting enzyme Caspase-3, resulting in morphological collapse and cell apoptosis. Similarly, LPS induced pro-inflammatory response and the production of pro-inflammatory factors TNF-α, IL-6, IL-1β and NOS2 and inhibition of cell viability. Edaravone is an antioxidant and radical scavenger. Its medication reactivates Akt signaling axis, rescues the expression of anti-apoptotic protein Bcl-2, and inhibits Caspase-3, finally affords neuroprotective functions.