Intrarectal effect in the experimental colitis model and

Intrarectal
administration of acetic acid releases acetate ions, which results in massive
intracellular acidification that in turn damages epithelial cells. This is
associated with marked inflammatory response as evident by intense inflammatory cells
infiltrations into colonic tissues with subsequent release of pro-inflammatory
cytokines (Fabia et al. 1992; Kandhare et al. 2013). Consistently, the
present study showed that administration of acetic acid caused extensive
macroscopic and microscopic damage of the colon with significant increases in
colonic MPO activity as well as in TNF-? and IL1ß expressions. sod sel
treatment was effective in reducing macroscopic damage score, total histology
score, MPO activity and the inflammatory cytokines expression.

It
was described that ROS (reactive oxygen species) produced in the inflamed
mucosa can moderate many inflammatory events. ROS produce several inflammatory
cytokines in various tissues which exacerbate tissue damage. In the present
investigation, acetic acid administration induced marked oxidative stress that
was associated with marked depletion of the cellular antioxidant, GSH as was
reported in earlier studies
(Nieto et al. 2000).

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The
activities of the antioxidant enzymes, SOD and catalase were also reduced in
acetic acid control rats. Such effects have also been reported in experimental
colitis (Boots et al. 2008). The free radicals formed during
oxidative damage target polyunsaturated fatty acids in plasma membrane leading
to membrane lipid peroxidation and severe cell damage. This interaction has an important
role in the pathogenesis of the disease In this study colitis control animals demonstrated
increased MDA levels in colon tissue. Sod sel treatment significantly reduced
the elevated MDA levels. A significant reduction in MDA by treatment with sod
sel shows the anti-inflammatory effect in the experimental colitis model and
this may be associated with the antioxidant and free radical scavenging ability
of sod sel. GSH is an important intracellular
antioxidant agent in mammalian gut. It is involved in the repair mechanism as
it inhibits mucosal damage induced by free radicals. During inflammation, GSH
level decreases resulting in severe degradation of colon mucosa. Therefore, GSH
plays an important role in protecting the intestinal cells and as a defense
mechanism against inflammation (Schreck et al. 1991). Treatment with sod sel significantly increased the colonic
GSH level that reasonably resulted in mitigation of macroscopic and
histopathologic indices.

NO
is an important proinflammatory mediator. The nitric oxide has been reported as
potential mediators for colitis (Whittle 1997). The detected
inflammatory reactions as higher interstitial edema, increased arteriolar blood
flow, fluid exudation across intestinal capillaries, thickening of the
intestinal wall, are all associated with inflammatory mediators such as NO (Whittle 1997). The
present study showed that administration of sod sel significantly inhibited NO
production which prevented peroxynitrite formation from inflammatory cells and
Countered inflammation.

Ulcerative colitis has been associated with an intense local
immune response which is associated with recruitment of lymphocytes and
macrophages followed by release of soluble cytokines. Cytokines are crucial
elements in gastrointestinal inflammation, however, their overproduction result
in injurious events. TNF and IL1? are important proinflammatory cytokines
released from the macrophages and lymphocytes in the early inflammatory
response (Fuss et al. 1996).

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