Fig. 5

Protective effect of CDNVs in ox-LDL-treated HUVECs. A Confocal microscopy images were used to show the uptake of CDNVs by HUVECs, with a scale bar representing 100 μm. B The effect of CDNVs (40 µg/ml) on HUVEC proliferation was evaluated using a CCK-8 assay at different treatment durations. C The effect of CDNVs (0, 0.4, 4, 40, 80 and 160 µg/ml) on HUVEC proliferation was evaluated at different concentrations using a CCK-8 assay. D The effect of CDNVs (40 µg/ml) and HSYA (0.27 µg/ml) on HUVEC proliferation was compared using a CCK-8 assay. E The effect of CDNVs (40 µg/ml) and HSYA (0.27 µg/ml) on the proliferation of ox-LDL-treated (100 µg/ml) HUVECs was compared using a CCK-8 assay. F-G The effect of CDNVs (40 µg/ml) and HSYA (0.27 µg/ml) on ox-LDL-induced (100 µg/ml) apoptosis in HUVECs was evaluated and statistically analysed. H The effect of CDNVs (40 µg/ml) and HSYA (0.27 µg/ml) on the level of ROS in ox-LDL-treated (100 µg/ml) HUVECs was measured. I-J Fluorescence microscopy images were used to show the adhesion of monocytes to HUVECs, with a scale bar representing 500 μm, and the results were statistically analysed. K The levels of VCAM-1 and ICAM-1 proteins in HUVECs were analysed using Western blotting. L The levels of VCAM-1 and ICAM-1 proteins in HUVECs, as normalized to GAPDH, were quantified. M qPCR assays were conducted to measure the mRNA levels of VCAM-1 and ICAM-1 in HUVECs, and the results were quantified and normalized to GAPDH. The results represent three independent experiments (n = 3). Data represent means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001