MEs inhibit proinflammatory factors by suppressing MAPKs and NF-κB activation in the activated microglia. (a–c) MEs inhibited LPS-induced NO (a), TNF-α (b), and IL-6 (c). BV2 cells were treated with LPS (200 ng/mL) and indicated concentrations of MEs. After 24 h treatment, NO, TNF-α, and IL-6 in the supernatant were measured; data are expressed as mean ± SD. (d) The endpoint microscope immunofluorescence image of Iba-1 in BV2 cells. BV2 cells were treated with LPS (200 ng/mL) and indicated concentration of MEs for 24 h. Iba-1 immunofluorescence staining was subsequently performed. Scale bar = 100 μm. (e, f) Effect of MEs on the LPS-induced phosphorylation of p65, ERK, JNK, and p38. BV2 cells were treated with LPS (200 ng/mL) and indicated concentrations of MEs for 1.5 h. Cell lysates were prepared, and the protein samples were analyzed by western blot analysis. TAK-242 (1 μM), a classic TLR4 antagonist, was used as the control. Results are representative of those obtained from three independent experiments.