Fig 1.
Structural formulas of V, AV and BAV.
Fig 2.
Schematic representation of acevaltrate degradation (AVD).
Table 1.
MS and MS/MS spectroscopic data for the iridoid valepotriates and their degradation products.
Table 2.
Antioxidant effect of the iridoid valepotriates assessed through ABTS and DPPT• assays.
Table 3.
Cytotoxicity of iridoid valepotriates against HepG2, HeLa and MDA-MB-231 cells and HUVECs.
Fig 3.
Effect of V, AV, BAV and their degradation products on ROS in HepG2 cells.
ROS in the cells was labelled with DCFH-DA and measured by flow cytometry. (A—G) Results for the (A) control, (B) V (-20°C), (C) V (25°C for 7 days), (D) AV (-20°C), (E) AV (25°C for 7 days), (F) BAV (-20°C) and (G) BAV (25°C for 7 days) groups. (H) The data are presented as the means ± SDs from three separate experiments (* p < 0.05).
Fig 4.
Apoptosis was measured by flow cytometry through Annexin V-FITC and PI staining.
Representative plots from one set of Annexin V-FITC flow cytometry and PI staining experiments performed in triplicate are shown. Early apoptotic cells (Annexin-V+ and PI-) are shown in the lower right quadrant, and late apoptotic cells (Annexin-V+ and PI+) are shown in the upper right quadrant. The percentages of apoptotic cells are indicated as Annexin-V+ cells and are shown as the means ± the SD from three independent experiments. (A—G) Results from the (A) control, (B) V (-20°C), (C) V (25°C for 7 days), (D) AV (-20°C), (E) AV (25°C for 7 days), (F) BAV (-20°C) and (G) BAV (25°C for 7 days) groups. (H) The data are presented as the means ± the SD from three separate experiments (* p < 0.05).
Fig 5.
Proposed mechanism for the DPPH• reaction.
Fig 6.
Proposed interactions between valepotriates and the GABAergic signalling pathway.