Fig. 9.

Effects of rivaroxaban and a PAR2 antagonist on fibrosis and inflammation in cardiac fibroblasts

Cardiac FBs exposed to hypoxia were treated with or without a PAR2 antagonist, FSLLRY (10 µM) for 24 hours or rivaroxaban (2 µg/ml) for 24 hours or FSLLRY (10 µM) for 24 hours, subsequently changed to rivaroxaban (2 µg/ml) for 24 hours. (A) The elevated expression level of PAR2 induced by hypoxic stimulation was downregulated by rivaroxaban or the PAR2 antagonist FSLLRY, or both. (B, C) The mRNA expressions of MMP9 and COL-1 in cardiac FBs were attenuated by the presence of rivaroxaban or FSLLRY or both. (D–F) The mRNA expressions of pro-inflammatory genes IL-6, IL-1β, and TNF-α were reduced by the presence of rivaroxaban or FSLLRY or both (n = 3–5 per group). *p < 0.05, **p < 0.01, and ***p < 0.001. Riv: rivaroxaban.