Conclusions: LcrV-secreting L lactis decreased experimentally induced intestinal inflammation in 2 murine models of colitis.
Using staining techniques to visualize hypoxic foci, a robust increase in hypoxia is observed in mouse models of colitis [2].
Lastly, the temporal regulation of HIF-1α and HIF-2α has not been critically assessed in chronic models of colitis.
Currently, the pan-PHD inhibitors dimethyloxaloylglycine, FG-4497, and TRC160334 are protective in mouse models of colitis [14, 15, 22].
Discussion: This model may be used as an alternative or a complement to chemical models of colitis.
However, expression of pro-inflammatory mediators is significantly increased, and the mice are highly susceptible to inflammatory injury in mouse models of colitis.
Recombinant lactococci and lactobacilli strains expressing antiproteases and antioxidant enzymes have been tested successfully for their prophylactic and therapeutic effects in murine models of colitis.
In rodent experimental models of colitis, a decreased expression of K ATP) channels (Subunits: Kir6.1/6.2 and SUR1/2) is reported.
Our aim was to design a new formulation based on silver and validate its anti-inflammatory activity in the mouse models of colitis.
Another study reported that dysbiosis observed in murine models of colitis is associated with composition change of bacteria present in the oral cavity and in saliva (Said et al., 2014; Lucas López et al., 2017).
Currently, these drugs have not been assessed in mouse models of colitis, but the data suggest that disruption of intestinal epithelial HIF-2α decreases the inflammatory response in colitis [8].
