Fig 1: Blockage of FABP2 suppresses HFHC diet–induced intestinal permeability in ApoE-/- mice. Male ApoE-/- mice were fed with HFHC for 12 wk, then treated with 1 × 109 lentiviral particles encoding villin-drived Fabp2 siRNA or control siRNA (Veh) for 8 wk. A, Haematoxylin and eosin staining of small intestine. Scale bar = 100 µm. B-C, Real-time PCR analysis of intestinal zonula occludens (ZO)-1 (B) and occludin (C) levels. D-F, Western blot analysis of ZO-1 and occluding (D), and quantitative analysis of relative density of ZO-1/Tubulin (E) and occluding/Tubulin (F). G, Serum levels of lipopolysaccharides (LPS). H, The circulating concentration of DX-4000-FITC after mice was orally administrated with FITC-labelled dextran. Data are shown as mean ± SEM (*P < .05, **P < .01 and ***P < .001, Student's t test was used for 2-group comparison, n = 6-7 mice/group)
Fig 2: Circulating FABP2 is closely correlated with atherosclerotic parameters in clinical patients. A, The plasma FABP2 levels in 18 patients with carotid intima-media thickness (IMT) = 0.85 mm and 24 patients with IMT < 0.85 mm. B-D, The correlation between circulating levels of FABP2 and IMT (B), total cholesterol (C) and triglyceride (D). Data are shown as mean ± SEM (**P < .01, Student's t test was used for 2-group comparison, and Pearson's analysis was used for the correlation)
Fig 3: Blockage of FABP2 attenuates HFHC diet–induced atherosclerotic progress in ApoE-/- mice. Male ApoE-/- mice were fed with HFHC for 12 wk and then treated with 1 × 109 lentiviral particles encoding villin-drived Fabp2 siRNA or control siRNA (Veh) for 8 wk. A-B, Representative images of Oil Red O staining of En Face aorta (A) and quantitative analysis of relative density (B). C-D, Oil red O staining of aorta root (C) and quantitative analysis of relative lipid deposits (D, red colour area). Scale bar = 100 µm. E-H, Slides of aorta root were stained with moma-2 and a-sma antibodies, or trichrome staining solution. Representative images of staining (E), and quantitative analysis of relative density of aorta moma-2 (F), a-sma (G) and collagen (H). Scale bar = 50 µm. I-M, Real-time PCR analysis of aorta gene expression of Tnf-a (I), Il-1ß (J), Mcp-1 (K), Vcam-1 (L) and Icam-1 (M). Data are shown as mean ± SEM (**P < .01 and ***P < .001, Student's t test was used for 2-group comparison, n = 5-7 mice/group)
Fig 4: High-fat high-cholesterol diet increases the level of FABP2 in ApoE-/- mice. A, The distribution of Fabp2 in aorta, heart, kidney, visceral fat and small intestine of ApoE-/- mice fed with standard chow for 12 wk. B, Male ApoE-/- mice were fed with high-fat high-cholesterol diet (HFHC) for 0, 4, 12 and 20 wk. The Fabp2 expression in small intestine. Data are shown as mean ± SEM (**P < .01 and ***P < .001, anova analysis was used for multiple group comparison, n = 5 mice/group)
Fig 5: Blockage of FABP2 inhibits intestinal inflammatory response in ApoE-/- mice. Male ApoE-/- mice were fed with HFHC for 12 wk and then treated with 1 × 109 lentiviral particles encoding villin-drived Fabp2 siRNA or control siRNA (Veh) for 8 wk. A-E, Real-time PCR analysis of inflammatory gene expression on small intestine. F-H, Intestinal production of TNF-a, IL-1ß and MCP-1. Small intestine was collected and homogenized, and the levels of cytokines TNF-a (F), IL-1ß (G) and MCP-1 (H) were measured by ELISA. Data are shown as mean ± SEM (*P < .05, **P < .01 and ***P < .001, Student's t test was used for 2-group comparison, n = 6-7 mice/group)
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