**Figure 8.** *Cont*.

**Figure 8.** Effect of HLP on atherosclerotic lesions, and VSMC migration and proliferation in vivo. Among five groups, New Zealand white rabbits fed on a high-fat diet (HFD) were divided into three groups. At the same time, two of the groups were orally treated with HLP at a dose of 0.5% or 1.0%. These rabbits were sacrificed after 25 weeks. The serum levels of triglycerides (TG), total cholesterol (CHO), low-density lipoprotein cholesterol (LDL-c) (**a**), ratio of LDL-c/ high-density lipoprotein cholesterol (HDL-c) (**b**), and TNF-α (**c**) were determined by ELISA assays. The results are presented as mean ± SD from one independent experiment. # *p* < 0.05, ## *p* < 0.01 compared with the control. \* *p* < 0.05, \*\* *p* < 0.01 compared with the HFD group. The aortic arches were collected for (**d**) oil red O stain, (**e**) immunohistochemistry (IHC) staining of α-SMA (upper panel), PCNA (lower panel). Images were taken at 400× magnification; scale bar, 50 μm. (**f**) Western blot analysis of MMP-9, p-Akt, Akt, E2F, p-p53, and p53 protein expressions was carried out with the tissue extracts from them. β-actin was served as an internal control. Results are representative of at least three independent experiments. +, added; −, non-added. (**g**) Overview of pathways for the proposed mechanism of HLP-induced inhibition of atherosclerosis in rabbits and VSMC migration/proliferation.
