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©The Author(s) 2025.
World J Gastroenterol. Mar 14, 2025; 31(10): 100194
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.100194
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.100194
Figure 7 Inhibition of vascular endothelial growth factor C/vascular endothelial growth factor receptor 3 reverses the amelioration of intrahepatic angiogenesis and inflammation by platelet-rich plasma-induced platelets.
A: Representative immunohistochemistry images of von Willebrand factor (vWF), matrix metalloproteinase 2 (MMP2), vascular endothelial growth factor A (VEGF-A), cluster of differentiation 31 (CD31) and CD68 in the livers of different groups; Quantitative analysis of B: vWF; C: MMP2; D: VEGF-A; E: CD31; 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; VEH: Vehicle.
- Citation: Chen M, Zhao JB, Wu GB, Wu ZH, Luo GQ, Zhao ZF, Zhang CH, Lin JY, Li HJ, Qi XL, Huo HZ, Tuersun A, Fan Q, Zheng L, Luo M. Platelet activation relieves liver portal hypertension via the lymphatic system though the classical vascular endothelial growth factor receptor 3 signaling pathway. World J Gastroenterol 2025; 31(10): 100194
- URL: https://www.wjgnet.com/1007-9327/full/v31/i10/100194.htm
- DOI: https://dx.doi.org/10.3748/wjg.v31.i10.100194