Localization and Expression Level of Vascular Endothelial Growth Factor after Partial Hepatectomy of WKY Rats

Inflammation and fibrosis are indicative of liver regeneration following injury and chronic liver diseases, such as cirrhosis and hepatocellular carcinoma. The formation of new vasculature via the process of angiogenesis is vital to the pathological progression of liver regeneration and these diseases. Thus, inhibiting the process of angiogenesis could have the potential to stop or slow the progression of chronic liver diseases. Vascular endothelial growth factor (VEGF) is the most potent and specific growth factor for initiating the process of angiogenesis, making it a prime target to inhibit angiogenesis. Bevacizumab is an antibody that binds to VEGF, inhibiting it from initiating angiogenesis. To investigate the effect that bevacizumab had on VEGF, we determined the localization and expression levels of VEGF after partial hepatectomy in Wistar-Kyoto rats using quantitative immunofluorescence. The tissue samples (n=5) consisted of four groups. Group 1 received no treatment and served as the negative control. Group 2 received bevacizumab treatment without hepatectomy and group 3 had a hepatectomy without bevacizumab treatment. Groups 2 and 3 served as controls to bevacizumab treatment and hepatectomy, respectfully. Group 4, the experimental group, had both hepatectomy and bevacizumab treatment. Western Blot analysis confirmed a significant increase in the level of VEGF in rats receiving partial hepatectomy treatment only. To determine the expression level of VEGF in cells/tissues, we prepared cryosections and probed with a fluorescently labelled anti-VEGF. Digitized images were captured using Simple PCI and localization pattern and expression level determined. Our results have broadened our understanding of chronic liver diseases