In addition, since the overproduction of ROS triggered by LPS was ameliorated by IOE treatment in C6 glioma cells, our data suggest that IOE may target the TLR-4/MyD88/ROS/MAPKs or TLR-4/MyD88/ROS/NFκB pathways to prevent LPS-induced neuroinflammation (Figure 11). This evidence concerns the gene TLR4 and glioma.