Aim: To
investigate the effect of balsalazine treatment on
intestinal mucosal permeability in dextran sulfate
sodium (DSS)-induced colitis and to determine the mechanism of the balsalazine-induced changes.
Methods: Experimental colitis was induced in C57BL/6J mice by the
administration of 5% DSS. Balsalazine was administered intragastrically at doses of 42, 141, and 423 mg/kg. The disease activity index (DAI) score was evaluated and colon tissue
was collected for the assessment of histological changes. The amount of malondialdehyde (MDA) in the colon was determined, along with the activity of myeloperoxidase (MPO), superoxide dismutase (SOD) and
glutathione peroxidase (GSH-Px). Mucosa from the small intestine was
collected to determine the levels of tumor necrosis factor (TNF)-α and
interferon (IFN)-γ. The mucosa was ultrastructurally examined with transmission electron
microscopy and intestinal permeability was assayed using Evans blue.
Results: Balsalazine was
found to reduce the DAI score and the histological index (HI) score, decrease
the MDA content and the activity of MPO, and increase the activity of SOD and
GSH-Px in colitis mice. At the same time, balsalazine ameliorated microvillus and tight junction structure, resulting in a decrease
in the amount of Evans blue permeating into the intestinal wall and the levels
of TNF-α and IFN-γ in colitis mice.
Conclusion: In colitis mice, the anti-colitis effect of balsalazine results in a decrease in intestinal mucosal permeability. The mechanism of this effect is partly
associated with balsalazine’s antioxidative and anti-inflammatory effects.
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