Twelve weeks of nCUR treatment in rats with chronic GWI reduced oxidative stress, improved mitochondrial function, and repressed proinflammatory cytokines and chemokines in the hippocampus. The bar charts in A-D compare the concentration of malondialdehyde (MDA; A), protein carbonyls (PCs; B), the nuclear factor erythroid 2-related factor 2 (NRF2; C), and superoxide dismutase (SOD; D) in the hippocampus between naïve, and GWI rats receiving vehicle (GWI-VEH) or nCUR (GWI-nCUR). Note that MDA and PCs were upregulated, and NRF2 and SOD were downregulated in the GWI-VEH group, compared to the naïve control group. In the GWI-nCUR, all four markers were normalized to naïve control levels. The bar charts E-I compare the expression of genes Ndufs6 (E), Bcs1l (F), Cyc1 (G), Cox6a (H), and Atp6ap1 (I) between different groups. These genes' expression was downregulated in the GWI-VEH group but normalized to naïve control levels in the GWI-nCUR group. The bar charts in J-M compare the concentration of mitochondrial complexes I-IV in the hippocampus between different groups. The bar charts in N-U compare the concentration of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein 1 alpha (MIP-1α or CCL3), interleukin-15 (IL-15), transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), fibroblast growth factor-beta (FGF-β) and Leptin in the hippocampus between different groups. All of these cytokines and chemokines except IL-1β and TGF-β were upregulated in the GWI-VEH group but significantly reduced in the GWI-nCUR group. *, p<0.05, **, p<0.01, ***, p<0.001, and ****, p<0.0001; NS, not significant.