Preventive Effect and Mechanism of Crossostephium chinense Extract on Balloon Angioplasty-Induced Neointimal Hyperplasia

Figures

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  Figure 1. HPLC fingerprinting profiles of three different CCEs. (a) CCE1. (b) CCE2. (c) CCE3.

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  Figure 2. Inhibitory effects of CCE3 on VSMC growth and migration. Cell viability (a) and cell migration (b) were analyzed using MTT and transwell assays, respectively, in A10 cells treated with several concentrations of CCE3. ∗P < 0.05 and ∗∗P < 0.01 compared with the control group (10% FBS alone group).

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  Figure 3. Regulation of growth- or migration-associated molecules by CCE3. A10 cells were starved for 24 h and then stimulated with 10% FBS for 30 min in the presence of various concentrations (1, 2, and 4 μg/mL) of CCE3 to examine the phosphorylation levels of detected proteins (a) or to analyze the total levels of detected proteins after 24 h of incubation (b). ∗P < 0.05 and ∗∗P < 0.01 compared with the group treated with 10% FBS alone.

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  Figure 4. Regulation of LPS-induced inflammatory molecules by CCE3. RAW264.7 cells were incubated with several concentrations (2, 4, and 8 μg/mL) of CCE3 in the presence of 20 ng/mL LPS to examine the expression levels of LPS-stimulated inflammatory enzymes at translation levels (a) and that of cytokines at transcriptional levels (b). The expression level of miRNA-132 was analyzed in A10 cells after 24 h of treatment with CCE3 (c). ∗P < 0.05 and ∗∗P < 0.01 relative to the group treated with LPS alone. †P < 0.05 relative to the control group (10% FBS alone).

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  Figure 5. Preventive effect of CCE3 on balloon-induced neointima formation. Artery cross-sections were cut using a cryostat and stained with hematoxylin and eosin to examine histopathological changes in arteries by using a microscope at 100-fold (upper panel) and 200-fold magnification (lower panel), respectively (a). L, lumen; N, neointima; M, media. Severity of neointimal hyperplasia was quantified by determining the ratio of the neointima-to-media area (N/M ratio) (b). ∗∗P < 0.01 compared with the BI group.

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  Figure 6. Schematic overview of the pharmacological mechanism of CCE3 in the prevention of neointimal hyperplasia.