Fig. 5.

S-allylcysteine (SAC) consumption induced the neovasculogenesis and increased c-kit protein level in animal models. To develop a negative control subgroup, endothelial progenitor cells (EPCs) alone were transplanted into the nude mice. For the positive control subgroup, EPCs were mixed with stem cell factor (SCF; 20 ng/mL) and subcutaneously inoculated into mice. For the experimental subgroups, nude mice were inoculated with EPCs and received low dosage (low SAC; 0.2 mg/kg of body weight [BW] per day) or high dosage (high SAC; 2 mg/kg of BW per day) of SAC by gavage (oral tube feeding) for 2 wk. The neovascularization samples from experimental animals were sectioned and treated with anti-c-kit antibody by immunohistochemistry staining. Imaging was documented at 200× (A) and 400× (B) magnification. Intense dark brown indicates the distribution of c-kit protein during neovasculogenesis. The formation of vascular vessel was indicated with a yellow arrow. EPCs were indicated with a blue arrow. The quantitative results (mean ± standard deviation) of the c-kit+ expressing cells were analyzed by using1-way analysis of variance and shown in the bottom panel (C). Different letters indicate a significant difference among different subgroups (P < 0.05). Hematoxylin and eosin staining of liver tissues was observed and documented at 200× (D) and 400× (E) magnification in any of the mice receiving SCF (20 ng/mL) or SAC (either 0.2 or 2 mg/kg of BW).