Fig 1: DHA protects dual gut barrier function in colitis. A) Flowchart of animal experiment modeling process. B) Representative images of tight junctions in colonic tissue from each group of mice by transmission electron microscopy (TEM). Red arrows indicated sites of tight junctions. C) Representative immunofluorescence images of PV1 (red) expression on colonic vessels stained with CD31 (green) in each group. DAPI (blue) stained cell nuclei. Quantification of CD31+ cells D), PV1+ cells E), and CD31+/PV1+ cells F) in colon tissue from each group. About 50 cells were surveyed in each sample, and five fields of vision were used for quantification. G) The integrity of the GVB was assessed by measuring the fluorescence intensity of FD70 (green), referring to the emergence of FD70 in the liver and spleen after gut lumen exposure to FD70 in different groups. Quantification of fluorescence intensity of FD70 in the spleen H) and liver I) from each group. J) Experimental illustration of DHA's impact on IEB/GVB via EGCs modulation under inflammatory conditions. K‐L) Western blot analysis of the level of IEB barrier proteins (ZO‐1, Occludin, Claudin‐2, and Claudin‐1) in HT29 under EGCs conditioned medium treatment with or without DHA therapy under inflammatory conditions. M‐N) Western blot analysis of the level of GVB barrier proteins (ZO‐1, β‐catenin, Occludin, PV1, Claudin‐2, and Claudin‐1) in HUVECs under EGCs conditioned medium treatment with or without DHA therapy under inflammatory conditions. DHA, dihydroartemisinin; DSS, dextran sulfate sodium; DAPI, 4′,6′‐diamidino‐2‐phenylindole; FD70, FITC‐labeled fluorescent dextran 70 KDa; IEB, intestinal epithelial barrier; GVB, gut vascular barrier; EG‐CM, enteric glial‐conditioned medium; EGCs, enteric glial cells. Scale bars are shown in the figures. n = 5 for each group (B, C, and G). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.