Fig 2: Construction a biomimetic nano-drug treat homocysteine (Hcy)-induced atherosclerosis by inhibiting macrophage pyroptosis. Additionally, this nano-drug improves the dysbiosis of gut microbes while reducing the inflammatory response and blood Hcy levels. PB: Prussian blue; NPs: nanoparticles; RVS: rosuvastatin; PR: RVS-loaded PB; MPR: macrophage membrane-coated PR; ZO-1: zonula occludens-1; ROS: reactive oxygen species; HIF-1α: hypoxia-inducible factor-1α; TLR4: Toll-like receptor 4; NF-κB: nuclear factor kappaB; NLRP3: oligomerization domain (NOD)-like receptor thermal protein domain associated protein 3; IL: interleukin; GSDMD: gasdermin D; N-GSDMD: N-terminal GSDMD.

Fig 3: Macrophage membrane (Møm)-coated rosuvastatin (RVS)-loaded Prussian blue (PB) nanoparticles (MPR NPs) inhibited pyroptosis in atherosclerosis plaque of apolipoprotein E knockout (ApoE−/−) mice fed an high methionine diet (HMD). (A, B) Immunohistochemistry staining with antibody to hypoxia-inducible factor-1 (HIF-1α) (A) and quantitative analysis (B) of aortic roots. (C) Immunofluorescence images of nucleotide-binding and oligomerization domain (NOD)-like receptor thermal protein domain associated protein 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) colocalization. (D) Pearson product-moment correlation coefficient analysis (PCCs) of NLRP3 (red) and ASC (green) colocalization. (E) Immunofluorescence images of cleaved-gasdermin D (C-GSDMD) and F4/80 levels. (F) Fluorescence intensity of C-GSDMD/F4/80. The above experiments were performed on HMD-induced ApoE−/− mice treated with PB NPs, RVS, and MPR NPs. Data are means ± standard deviation (SD) (n = 3). ###P < 0.001 vs. the control group; ∗∗P < 0.01 and ∗∗∗P < 0.001 vs. the HMD. DAPI: 4′,6-diamidino-2-phenylindole.