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To induce the murine colitis, we followed the procedures described by Wirtz S et al.[ 22].
To assess the effects of IL-4 or/and IL-10 expression on treatment of TNBS-induced murine colitis, we intraperitoneally injected these plasmids into mice and then detected these transgenic expressions in murine colon tissues using qRT-PCR.
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We induced murine colitis by intrarectal administration of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS).
To investigate the effects of local administration of IFN-β on a murine model of colitis, we developed a transgenic Lactobacillus acidophilus strain that constitutively expresses IFN-β (La-IFN-β).
Based on its anti-inflammatory properties and previous success in colitis studies, we investigated the effects of IFN-β in a murine colitis model.
In the current study, we investigated the effects of L. japonica on experimental murine colitis.
In this study, we examined the effect of A2B receptor antagonism on murine colitis.
To further confirm the therapeutic effect of IL-4 and IL-10 gene therapy, we performed qRT-PCR analysis of their expression in TNBS-induced murine colitis tissues.
In the light of the increased IL34 and CSF1 expression in the inflamed intestine of patients with IBD, we next assessed their involvement in the widely used DSS model of murine colitis [ 25].
We established that netrin-1 expression was enhanced within the colonic mucosa during murine colitis.
We evaluated the contribution of colonic inflammation to osteopenia and its mechanism in a murine colitis model.
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