Purpurin, a natural product isolated and purified from the herbs of Rubia cordifolia L. with antifungal activity, suppresses C. albicans morphogenesis and causes distorted biofilm formation, and is a specific inhibitor of Adipocyte-derived leucine aminopeptidase and could be developed as an anti-angiogenic agent.
Purpurin is a natural anthraquinone compound from Rubia tinctorum L. Purpurin (Orally; 2, 6, 18 mg/kg for 3 weeks) exerts dose-dependently antidepressant-like effects on behavior and stress axis reactivity in adult male C57BL/6J mice (6-7 weeks old upon arrival) [3]. In vitro enzymatic analyses demonstrated that purpurin inhibited A-LAP (Adipocyte-derived leucine aminopeptidase) activity in a non-competitive manner with a Ki value of 20 M. In angiogenesis assays, purpurin inhibited the vascular endothelial growth factor (VEGF)-induced invasion and tube formation of human umbilical vein endothelial cells (HUVEC) [4]. Purpurin was non-toxic when fed to Drosophila and it significantly ameliorated the AD-related neurotoxic symptoms of transgenic flies expressing WT-FL (full-length) human Tau (hTau) plausibly by inhibiting Tau accumulation and reducing Tau phosphorylation. Purpurin also reduced hTau accumulation in cell culture overexpressing hTau. Importantly, Purpurin efficiently crossed an in vitro human blood-brain barrier model[5]. The administration of purpurin at 50 and 100 μM in 3T3-L1 cells, and at 40 and 80 mg/kg in mice proved to be a sensitive range: the lower concentrations affected several measured parameters, whereas at the higher doses purpurin consistently mitigated biomarkers associated with adipogenesis, and weight gain in mice[6]. Moreover, purpurin (36 μM) exposed to HCT-116 cells and incubated for 24 and 48 h could induce reactive oxygen species production, subsequently alter mitochondrion membrane, and increase the apoptotic cells in HCT-116. And purpurin induces messenger RNA expression of apoptotic genes (Bax, CASP-9, and CASP-3) in HCT-116 cells[7].
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