Fig. 7.

MEL treatment to rats with chronic GWI diminished NLRP3 inflammasomes and reduced the concentration of multiple proinflammatory markers in the hippocampus. Figures A–R illustrate examples of NLRP3 inflammasomes in IBA-1+ microglia from the CA3 subfield of naïve control (A–C), GWI-Veh (D–F), GWI-MEL10 (G–I), GWI-MEL20 (J–L), GWI-MEL40 (M − O), GWI-MEL80 (P–R) groups. The bar charts in S-X compare concentrations of NF-kB (S), NLRP3 (T), caspase-1 (U), the number of inflammasomes/unit area (V), the percentage of microglia with inflammasomes (W), and IL-18 (X). These measures were upregulated in the GWI-Veh group but normalized to naïve control levels in the GWI-MEL groups. NF-kB was normalized in the GWI-MEL40-80 groups. NLRP3 was normalized in the GWI-MEL10-40 groups and reduced below the naïve control level in the GWI-MEL80 group. Caspase-1, the number of inflammasomes per unit area, and the percentage of microglia with inflammasomes were normalized in GWI-MEL10-80 groups. IL-18 was normalized in the GWI-MEL10-20 groups and reduced below the naïve control level in GWI-MEL40-80 groups. The bar charts in Y-AC compare the concentration of interleukin-1 beta (IL-1β; Y), tumor necrosis factor-alpha (TNF-α, Z), interferon-gamma (IFN-γ; AA), monocyte chemoattractant protein-1 (MCP-1; AB), macrophage inflammatory protein 1 alpha (MIP-1α; AC) between different groups assessed through a cytokine array. The bar charts AD-AE compare TNF-α (AD) and IFN-γ (AE) concentrations between different groups measured through individual ELISA. Compared to the naïve control group, TNF-α, IFN-γ, MCP-1, and MIP-1α were upregulated in the GWI-Veh group but normalized or reduced below the naïve control level in the GWI-MEL10-80 group. The concentration of IL-1β was reduced in the GWI-MEL40-80 groups compared to the GWI-Veh group. Scale bar, A-R = 25 μm; *, p < 0.05, **, p < 0.01, and ***, p < 0.001; NS, not significant.