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. 2016 Nov 7;6(4):1085–1095. doi: 10.5966/sctm.2016-0077

Figure 2.

Figure 2

Lipoxin A4, along with its precursors and ligand, were altered by hAECs. (A): Expression of the lipoxin A4 precursor genes ALOX‐5, ‐12, and ‐15 was increased at days 5 and 7 compared with saline controls (ALOX‐5: 0.393 ± 0.114 vs. 3.777 ± 1.98; ALOX‐12: 0.484 ± 0.248 vs. 1.520 ± 0.203; ALOX‐15: 0.020 ± 0.007 vs. 1.998 ± 0.983). ∗, p < .05. (B): Lipoxin A4 protein levels were elevated in lung lysates at day 7 in animals treated with hAECs compared with controls (0.103 ± 0.021 ng/ml vs. 0.249 ± 0.072 ng/ml, respectively). ∗, p < .05. (C): At day 7, bleomycin challenge resulted in positively stained F4/80/FPR2 cells, which were was elevated in mice treated with hAECs compared with control mice (5.720% ± 0.587% vs. 8.795% ± 0.687%, respectively). ∗, p < .05. (D): Representative images of F4/80‐ and FPR2‐positive‐stained lung sections from hAEC‐treated animals. Magnification: ×200. Scale bar =100 μm. Abbreviations: DAPI, 4′,6‐diamidino‐2‐phenylindole; FPR2, N‐formyl peptide receptor 2; hAEC, human amnion epithelial cell.