Fig. 3.
Fig. 3. Peptide Ac2-26 inhibition of the leukocyte-endothelium interaction in I/R-inflamed mesenteric vessels of FPR KO mice. / FPR KO mice were administered, through the jugular vein, PBS (100 μL; vehicle group, ▪), peptide Ac2-26 (100 μg corresponding to 33 nmol) alone (▧) or with Boc2 (10 μg corresponding to 12 nmol, ▨) at the beginning of the reperfusion period (ie, 30 minutes after ischemia), and mesenteries were analyzed 45 minutes later. A group of sham mice (■) was also included and analyzed 75 minutes after laparoctomy. The leukocyte-endothelium interaction was quantified in terms of (A) velocity of white blood cell rolling (expressed as VWBC); (B) number of adherent cells per 100 μm vessel length; and (C) number of emigrated cells per 100 × 50 μm2 area (see also Figure 1B). Data are mean ± SEM of n = 6 mice per group (n = 3 for sham group). Dotted lines highlight the sham values. *P < .5 versus respective vehicle-treated group.

Peptide Ac2-26 inhibition of the leukocyte-endothelium interaction in I/R-inflamed mesenteric vessels of FPR KO mice.

FPR KO mice were administered, through the jugular vein, PBS (100 μL; vehicle group, ▪), peptide Ac2-26 (100 μg corresponding to 33 nmol) alone (▧) or with Boc2 (10 μg corresponding to 12 nmol, ▨) at the beginning of the reperfusion period (ie, 30 minutes after ischemia), and mesenteries were analyzed 45 minutes later. A group of sham mice (■) was also included and analyzed 75 minutes after laparoctomy. The leukocyte-endothelium interaction was quantified in terms of (A) velocity of white blood cell rolling (expressed as VWBC); (B) number of adherent cells per 100 μm vessel length; and (C) number of emigrated cells per 100 × 50 μm2 area (see also Figure 1B). Data are mean ± SEM of n = 6 mice per group (n = 3 for sham group). Dotted lines highlight the sham values. *P < .5 versus respective vehicle-treated group.

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