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. 2017 Feb 21;6(4):e1293213. doi: 10.1080/2162402X.2017.1293213

Figure 2.

Figure 2.

Effects of FPR1 pharmacologic modulation on SPM biosynthesis. (A) EIA assays showing that fMLF (agonist to FPR1-10−9 M) treatment of AGS significantly increases RvD1 and LXB4 release compared to untreated cells (dotted line). In contrast, CsH (inverse agonist to FPR1-800 nM) treatment significantly reduced RvD1 and LXB4 release compared to controls (dotted line). Data are represented as mean ± SD of three independent experiments. *p < .05 compared to untreated cells. (B) fMLF induced, whereas CsH inhibited, ALOX5, ALOX15A, and ALOX15B mRNA expression in AGS and MKN45 cells. Data are represented as mean ± SD of three independent experiments. *p < .05 compared to untreated cells (dotted line). (C) fMLF induced, whereas CsH inhibited, ALOX5, ALOX15A, and ALOX15B protein expression in AGS cells, as evaluated by cytofluorimetric analysis. One representative experiment out of three is shown. (D) fMLF inhibited, whereas CsH induced, pro-angiogenic molecule mRNAs expression in AGS and MKN45 cells. Data are represented as mean ± SD of three independent experiments. *p < .05 compared to untreated cells (dotted line).