Fig. 5: Anti-atherosclerotic actions by MM-AT-NPs.

a DHE-stained sections of the aorta root, aorta arch and brachiocephalic artery, from atherosclerotic mice treated with various formulations (AT, AT-NPs, MM-AT-NPs, and AT-NPs/MAs) at a dose of 2 mg kg⁻¹ AT per week. Scale bar in aorta root and aorta arch: 400 μm. Scale bar in brachiocephalic artery: 800 μm. b Binding profiles of MM-NPs with TNF-α and IL-1β, MCP-1 (10 ng mL⁻¹ each), and oxLDL (20 μg mL⁻¹), with MM-NP varied from 0 to 4 mg mL⁻¹. Nonlinear regression fitting with inhibitory dose–response model (variable slope model) was employed to process data using Graphpad Prism 6. c, d MM-NP’s dose-dependent inhibition of macrophage inflammation induced by MCP-1 and oxLDL, respectively, with MM-NP varied from 0 to 4 mg mL⁻¹. e Representative microscopic images of ORO stained RAW264.7 cells treated with oxLDL (20 μg mL⁻¹) and MM-NPs (0.25, 0.5, 1, and 2 mg mL⁻¹, respectively). Scale bar: 50 μm. f Quantified contents of ORO in foam cells derived from RAW264.7 cells. The experiments were conducted for three times independently. All data were presented as mean ± s.d. Statistical analysis was conducted using one-way ANOVA. *P ≤ 0.05, **P ≤ 0.01, and ***P ≤ 0.001. For DHE-stained aorta tissues, n = 3 aorta tissues from different mice. For binding capacity, inhibition of macrophage inflammation and ORO stained RAW264.7 cells, n = 3 independent experiments using same batch of MM-NPs. IC₅₀ was calculated by variable slope model using GraphPad Prism 6. Source data are provided as a Source Data file.