attenuated the loss of intestinal barrier during DSS-induced colitis model. (A) Detection of viable bacteria in MLNs were shown for control group (a), model group (b) and 1,25(OH)2D3-treated group (c). (B) Differences in incidence of bacterial translocation were quantitated and shown, (C) Quantification of serum FITC-D, a measure of intestinal barrier function, was shown. (D) The levels of endotoxin were compared between control group, model group and 1,25(OH)2D3-treated group. Data were expressed as mean ± SD. a
P < 0.01 vs model group; b
P < 0.01 vs control group. (E) The ultrastructural features were observed by SEM. The colon mucosa in the control group was regular without histological lesion, (a, ×500; b, ×2 000); In the model group, the mucosa was severe loss, with histological lesions including crypt distortion and abscesses, (c, ×500; d, ×2 000); Areas with histological lesions in the 1,25(OH)2D3-treated group were significantly ameliorated; However, compared with the control group, there were less lesions and the crypt distortion and abscesses were less severer. Futhermore, crypt openings were disposed in rows. (e, ×500; f, ×2 000).