Platelet activation relieves liver portal hypertension via the lymphatic system though the classical vascular endothelial growth factor receptor 3 signaling pathway

Figure 8 Inhibition of vascular endothelial growth factor C/vascular endothelial growth factor receptor 3 reverses the amelioration of mesenteric angiogenesis and inflammation by platelet-rich plasma-induced platelets. A: Representative immunohistochemistry images of hematoxylin and eosin, lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1), vascular endothelial growth factor C (VEGF-C) and vascular endothelial growth factor receptor 3 (VEGFR-3) and cluster of differentiation 68 (CD68) in the mesentery of the different groups; Quantitative analysis of B: Wall thickness; C: LYVE-1; D: VEGF-C; E: VEGFR-3; F: CD68. The data represent the mean ± SD. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. BDL: Bile duct ligation; PRP: Platelet-rich plasma; SO-VEH: Sham-operated-vehicle; VEH: Vehicle.