L-Sepiapterin(Sepiapterin)是内皮型一氧化氮合酶(eNOS)辅因子四氢生物喋呤(BH4)的前体。L-Sepiapterin改善db/db小鼠肠系膜小动脉内皮功能障碍，诱导血管生成。L-Sepiapterin通过下调p70S6K依赖性VEGFR-2表达抑制卵巢癌细胞增殖和迁移。
L-Sepiapterin (Sepiapterin) is a precursor of the endothelial nitric oxide synthase (eNOS) cofactor tetrahydrobiopterin (BH4). L-Sepiapterin improves endothelial dysfunction in small mesenteric arteries from db/db mice, and induces angiogenesis. L-Sepiapterin inhibits cell proliferation and migration of ovarian cancer cells via down-regulation of p70S6K-dependent VEGFR-2 expression[1][2].
L-Sepiapterin (Sepiapterin) (0.1-10 μM; 24 hpurs) Iinduces cell proliferation in a dose-dependent manner[1].L-Sepiapterin (1-50 μM; 20 minutes) significantly inhibits the phosphorylation of VEGF-A-induced (50 ng/ml) p70S6K[1].L-Sepiapterin inhibits VEGF-A-induced cell proliferation and migration through NO-independent mechanism[1]. Cell Proliferation Assay[1] Cell Line: SKOV-3 cells
Sepiapterin (10 mg/kg; p.o. (powder chow); daily for or 8 weeks) significantly improves the relaxation to Ach in small mesenteric arteries (SMA) from db/db mice[2]. Animal Model: Male C57BL/KsJ diabetic mice (db/db)[2]
[1]. Pannirselvam M, et al. Chronic oral supplementation with sepiapterin prevents endothelial dysfunction and oxidative stress in small mesenteric arteries from diabetic (db/db) mice. Br J Pharmacol. 2003;140(4):701‐706. [2]. Cho YR, et al. Sepiapterin inhibits cell proliferation and migration of ovarian cancer cells via down-regulation of p70S6K-dependent VEGFR-2 expression. Oncol Rep. 2011;26(4):861‐867.
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