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Therefore, the effect of EPO on intestinal IR injury was examined by the change of intestinal histology; the expression of pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interferon γ (IFN-γ); and the protein levels of EPOR, p-EPOR, p85, p-p85, Akt, p-Akt, IκΒ-α, p-p65, and p65.
However, no change of intestinal metaplasia occurred in antrum and corpus of those with successful eradication.
At the same time, a change of intestinal flora can be detected, specifically with regard to adherent bacteria [ 2, 3].
The expression of intestinal FPN1 in 3 d and 7 d PS groups was lower than that of control, while the change of intestinal ferritin was opposite.
Therefore, upon a change of intestinal microbiota, it is suggested that both increased dietary fiber fermentation, and the induction of metabolic endotoxemia would lead to accumulate lipids in liver and trigger inflammation.
Furthermore, in animal models of obesity, induced by brain lesion of the ventromedial hypothalamus, a change of intestinal microbiota was also observed suggesting an important impact of the brain on the control of intestinal microbiota [ 55].
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Recent studies indicate that the changes of intestinal flora were closely associated with diabetes, obesity, hyperlipidemia, cardiovascular disease, colon cancer and other intestinal diseases.
The object of this study was to determine if GST levels correlated with histologic changes of intestinal ischemia in a controlled animal model of mesenteric intestinal ischemia.
This results in an increase in paracellular permeability and morphological changes of intestinal epithelial cells [49].
In addition to hepatic BA biosynthesis and cholestyramine-binding affinity, changes of intestinal microflora can also influence the bile acid profile in cholestyramine-fed mice.
Pathological changes of intestinal tissue were observed by light microscopy.
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