These effects are mediated through cell‐autonomous or non‐cell‐autonomous mechanisms after ischemic stroke.[158, 159] These dynamic changes depend on astrocyte interaction with microglia, neurons, and oligodendrocytes.[159, 160] Furthermore, reactive astrocytes release pro‐inflammatory cytokines, such as IL‐1β, IL‐6, and TNF‐α, actively participating in the inflammatory process after an ischemic stroke.[161, 162] Transient inhibition of mitochondrial complex I, achieved through Ginsenoside Rb1, can reduce mitochondrial ROS production, thereby preventing astrocyte activation. This evidence concerns the gene IL1B and ischemic stroke.