Fig 2: Diosmin maintains muscle function in a mouse model of iliac vein stenosis. (A) Gene ontology (GO) enrichment for the regulated genes in the surrounding muscles between the IVS/NS and IVS/diosmin (40 mg/kg) groups; n = 4 per group. (B) The relative protein levels of ICAM-1 and VCAM-1 in the surrounding muscles among the different groups: Sham/NS (n = 4), Sham/diosmin (40 mg/kg; n = 4), IVS/NS (n = 5), IVS/diosmin (20 mg/kg; n = 6), and IVS/diosmin (40 mg/kg; n = 8). *p < 0.05 vs. Sham/NS; #p < 0.05 vs. IVS/NS; &p < 0.05 vs. IVS/diosmin (20 mg/kg).

Fig 3: Loss of ATF3 aggravated the expression of inflammation-related genes in HFD-induced obese mice. a ATF3 protein level in iWAT and BAT of wild-type and ATF3−/− mice after HFD feeding for 12 weeks. b Representative immunofluorescence images of adiponectin (red IF) and ICAM-1 (green IF) in wild-type and ATF3−/− mice. Yellow scale bar indicated the size of adipocyte tissues. c Serum protein levels of adipokine and inflammation-related genes in wild-type and ATF3−/− mice after HFD feeding for 8 weeks by adipokine assays; Gel-Pro Analyzer software was used for densitometry of blots. d Serum protein level of adiponectin, ICAM-1 and resistin by ELISA assays in wild-type and ATF3−/−mice after HFD feeding for 8 weeks. e Quantified real-time PCR analysis of mRNA levels of iNOS, IL-6, and TNFα in livers of wild-type and ATF3−/− mice. For a–c, n = 3 per group. For d, wild-type (n = 4 in adiponectin; n = 5 in ICAM1; n = 8 in resistin), ATF3−/− (n = 7 in adiponectin; n = 5 in ICAM1; n = 7 in resistin). For e, n = 6 per group. Scale bar for image b: 50 µm. Data are mean ± SEM; *p < 0.05 compared to wild-type

Fig 4: Probiotics alleviate lipid accumulation and inflammation in HFD-fed ApoE−/− mice. (A) Oil Red O staining of aortic sinus sections in HFD and HFD + probiotics groups. (B-C) Immunohistochemical staining of CD68 and α-SMA in aortic root sections from HFD and HFD + probiotics groups. Serum levels of (D) TC, (E) TG, (F) LDL, and (G) HDL in HFD and HFD + probiotics groups. Serum levels of (H) IL-1β, (I) IL-6, (J) ICAM-1, and (K) VCAM-1 in HFD and HFD + probiotics groups. Data are shown as the mean ± SD from 7 mice per group, and statistical analyses were performed using unpaired Student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001

Fig 5: Circ_HUWE1 alleviates lipid accumulation and inflammation in HFD-fed ApoE−/− mice via the miR-143-3p/IGFBP5 axis. (A) Representative images of Oil Red O staining in aortic sinus sections and lipid deposition within lesion area from control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. (B-C) Immunohistochemical staining of CD68 and α-SMA. (D-G) Serum levels of TC, TG, LDL and HDL in control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. (H-K) Serum levels of IL-1β, IL-6, ICAM-1, and VCAM-1 in control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. Data are shown as the mean ± SD from at least three independent experiments, and statistical analyses were performed using one-way analysis of variance (ANOVA) with Tukey’s post-hoc test. *p < 0.05, **p < 0.01, ***p < 0.001