FIGURE 5.

Intestinal epithelium-specific PGC1α knock-out mouse (PGC1α^ΔIEC) was subjected to 2% DSS for 7 days along with PGC1α^loxP/loxP littermates (n = 8/group). When the % body weight was evaluated, significant differences were noted between PGC1α^ΔIEC control versus PGC1α^ΔIEC DSS-treated mice (#, p = ≤0.05), PGC1α^ΔIEC DSS versus PGC1α^loxP/loxP DSS-treated mice (*, p ≤ 0.05), and PGC1α^loxP/loxP control versus PGC1α^loxP/loxP DSS-treated mice ($, p ≤ 0.05) (A). DAI score for PGC1α^ΔIEC mice was significantly higher than that for PGC1α^loxP/loxP mice subjected to DSS colitis (B). Histologically, PGC1α^ΔIEC mice developed a more dramatic colitis, as quantified by average histology grade (C, scale bars, 100 μm). PGC1α^ΔIEC mice also demonstrated a significant increase in pro-inflammatory tissue cytokine release as compared with PGC1α^loxP/loxP mice (D). Activity of the electron transport chain complexes I and IV were significantly decreased in both strains of mice after DSS exposure. However, complex IV activity was significantly decreased in PGC1α^ΔIEC mice subjected to DSS as compared with PGC1α^loxP/loxP mice similarly treated (E). PGC1α^ΔIEC mice and PGC1α^loxP/loxP mice were subjected to a chronic model of 2% DSS exposure (n = 16/group). Significant differences in DAI were noted in the first two cycles of DSS treatment but not the third cycle (F). As seen after acute DSS colitis, PGC1α is decreased in the intestines of PGC1α^loxP/loxP mice after the completion of the chronic DSS model. *, p ≤ 0.05.