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Notoginsenoside Ft₁ is a saponin originally isolated from P. notoginseng with diverse biological activities. It induces proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) via nuclear translocation of hypoxia-inducible factor-1α (HIF-1α) and activation of the PI3K/AKT and Raf/MEK/ERK signaling pathways in a manner dependent on mammalian target of rapamycin (mTOR). Notoginsenoside Ft₁ (45 μM) induces cell cycle arrest at the S and G₂/M phases and promotes apoptosis of SH-SY5Y cells. It increases cGMP levels and induces relaxation of isolated precontracted rat mesenteric arteries, effects that are reversed by the nitric oxide synthase inhibitor L-NAME and ODQ , an inhibitor of soluble guanylyl cyclase. In vivo, notoginsenoside Ft₁ (0.25, 2.5, and 25 mg/kg) promotes angiogenesis and decreases wound diameter in a mouse model of punched-hole ear injury. Notoginsenoside Ft₁ (1.25 mg/kg) decreases tail bleeding time and increases thrombus weight in a rat tail bleeding assay. Topical administration of notoginsenoside Ft₁ increases mRNA expression of the collagen expression, fibroblast proliferation, and scar formation genes COL1A1, COL3A1, TGF-β1, TGF-β3, and fibronectin, promotes neovascularization, reduces monocyte infiltration, and shortens wound closure time in a db/db mouse model of diabetic foot ulcers.