The structural features of Aiphanol give it potent anti-angiogenic activity through the cooperation between its stilbene unit, the phenyl propane fraction and the dioxane bridge, in contrast to the mechanisms of stilbene or lignans. Drug combinations that inhibit VEGFR2 and COX2, respectively, have been shown to be effective in animal models of anti-angiogenic therapy. While inhibition of VEGFR2 in vitro primarily contributes to the anti-angiogenic function of Aiphanol, in vivo simultaneous inhibition of COX2 may reprogram the levels of PGE2 and VEGF by reducing the pro-angiogenic microenvironment. This study supports Aiphanol as a potential anti-angiogenic lead compound in cancer therapy.
Sarsaparilla aka Smilax Glabra Rhizome (SGR) has been extensively studied for its anti-tumor and anti-inflammatory potential, but its effect on angiogenesis has not been explored. Here, this study found that Glabrous Greenbrier Rhizome P.E inhibited the proliferation and motility of primary human umbilical vein endothelial cells (HUVEC). Importantly, Tu Fu Ling inhibited basal and growth factor-stimulated angiogenesis in angiogenesis assays, and this effect was dose-dependent. This study noted that Porphyra contains a number of compounds with anti-angiogenic abilities.
Aiphanol, originally isolated from the seeds of Aiphanes aculeate, was also identified in Glabrous Greenbrier Rhizome P.E. To date, the biological effects, including Aiphanol, are largely unknown. Aiphanol has been reported to inhibit angiogenesis in the rat aortic ring assay; however, the mechanism and its role in regulating tumour angiogenesis remain to be determined.
This study demonstrates that the naturally occurring lignan, Aiphanol, can directly target and inhibit VEGFR2 and COX2, thereby blocking angiogenesis and tumour growth. the structural features of Aiphanol give it potent anti-angiogenic activity through the cooperation between its stilbene unit, the phenyl propane fraction and the dioxane bridge, in contrast to the mechanisms of stilbene or lignan. Drug combinations that inhibit VEGFR2 and COX2, respectively, have been shown to be effective in animal models of anti-angiogenic therapy.
While inhibition of VEGFR2 in vitro primarily contributes to the anti-angiogenic function of Aiphanol, in vivo simultaneous inhibition of COX2 may reprogram the levels of PGE2 and VEGF by reducing the pro-angiogenic microenvironment. This study supports Aiphanol as a potential anti-angiogenic lead compound in cancer therapy.
