Skip to main content
. 2021 Mar 13;11(9):2859–2879. doi: 10.1016/j.apsb.2021.03.020

Figure 5.

Figure 5

FLZ administration attenuates systemic inflammation caused by increased intestinal inflammation and permeability in the rotenone-induced mouse model. (A) Levels of LPS endotoxin in the serum and feces. (B) Levels of LBP in the serum and feces. (C) Levels of LPS endotoxin in the colon. (D)–(F) Serum levels of IL-1β, IL-6, and TNF-α. (G)–(K) The mRNA expression of inflammatory markers (Cd3, Il1b, Il6, Cox 2, and Nos 2) in the colon. (L) Representative electron micrographs showing the tight junction structure of intestinal epithelium in the colon. (M) Concentrations of FITC in serum showing intestinal permeability. (N) Number of bacteria (CFUs) in the liver, spleen, and MLNs. (O) Representative captures of immunofluorescence in the colon of ZO-1. (P) ZO-1 integrity score in the colon. (Q) Representative Western blot brands of ZO-1, occludin and claudin-1 in the colon. (R) The density analysis results of ZO-1, occludin and claudin-1 Western blot in the colon. (S) The mRNA expression of tight junction proteins Zo1, Ocln and Cldn1 in the colon. In (A)–(F), n = 8 for each group. In (G)–(K), n = 3 for each group. In (M) and (P), n = 5 for each group. In (N), n = 6 for each group. In (R), n = 4 for each group. In (S), n = 3 for each group. Data are presented as mean ± SD. #P < 0.05, ##P < 0.01, ###P < 0.001 versus the Control group; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 versus the Rotenone group.