Edgeworthia gardneri (Wall.) Meisn. Attenuates Vascular Endothelial Cell Proliferation, Migration, and Angiogenesis

Angiogenesis, an essential process controlling the formation of new blood vessels, has been recognized to play a pivotal role in the pathophysiology of various diseases. A major cause of pathological angiogenesis is dysregulated vascular endothelial cell proliferation, migration, and tube formation. Edgeworthia gardneri (Wall.) Meisn. (EG), a well-known traditional Tibetan medicine, exhibits diverse pharmacological properties and has been shown to exert an endothelium-protective effect. However, its role in regulating endothelial cell-mediated angiogenesis has yet to be determined. Herein, a 30% ethanolic extract of EG (EEEG) is prepared and characterized as a promising anti-angiogenic agent. EEEG significantly inhibits endothelial cell proliferation, migration, and capillary-like tube formation in vitro. Using a syngeneic mouse tumor model, we demonstrate that EEEG suppresses angiogenesis in vivo, as reflected by reductions in both CD31-positive microvessel density and the expression of pro-angiogenic biomarkers within tumors. This anti-angiogenic effect may impair tumor growth in EEEG-treated mice. Furthermore, our study shows that EEEG’s mode of action on endothelial cells may be attributed to the attenuation of PI3K/AKT, JNK, and ERK signaling pathways. Collectively, these findings highlight the anti-angiogenic effect of EEEG and provide novel insights into its potential application in managing angiogenesis-dependent diseases.