We examined the effect of Bulnesia sarmienti (BS) water extract on hyperlipidemia induced by a high-fat diet. ICR mice were fed a high-fat diet ad libitum for four weeks. Simultaneously, BS water extract was administered intragastrically at 0 mg/kg (control), 30 mg/kg, or 300 mg/kg once daily for four weeks. Male ICR mice were divided into four groups; normal control group (NC), high-fat diet+vehicle treatment group (HF), high-fat diet+BS of 30 mg/kg treatment group (HF+BS30), and high-fat diet+BS of 300 mg/kg treatment group (HF+BS300). The levels of serum biochemical parameters and histological appearances were evaluated. After four weeks, body weight gain and serum levels of triglycerides, total cholesterol, and Low-density lipoprotein (LDL)-cholesterol were significantly higher in the HF group than in the normal control group. Together, serum High-density lipoprotein (HDL)-cholesterol level in the HF group was lower than that in the normal control group. However, treatment with BS resulted in significantly reduced body weight gain and levels of serum triglycerides, total cholesterol, and LDL-choleterol. In addition, serum HDL-cholesterol level in the BS treatment group was significantly elevated, compared to that of the HF group. Histopathological evaluation of the liver showed fat accumulation and swelling of hepatocytes in the high-fat diet group; these abnormalities were ameliorated by treatment with BS. These results suggest that treatment with BS water extract resulted in dose-dependent prevention and mitigation of high-fat diet-induced hyperlipidemia.

Sulfur is commonly used in Asia as an herbal medicine to treat inflammation and cancer , a nd potent chemo preventi ve effects have been demons tra ted in various in vivo and in vitromodels for s ul fur-containing compounds found in natura l1y occurring product s. Here, we 1'eport the growth inhibitory and apoptosis-related effects of a n ewly developedhigh-puri ty edible sulfur(ES) on immo1'tali zed human o1'al ke1'atinocytes(IHOKs) and on oral cancer cells representing two stages of oral cancer (HN4‘ HN12) based on an 3-(4,5-Dimethylthiazol-2-yl) -2.5- diphe n yltetrazolium bromide(MTI) assay, Western blotting, cell cycle analysis, and nuclear staining. The puri ty of the ES used in thi s study was ve1'ified by high performance liquid chromatog1'aphy (HPLC) , ami no acid analysis and energy dispersive spectroscopy(EDS). ES inhibited the prolife1'ation of imrnortalized and ma lig nant o1'al kerati nocytes in a dose- and time-dependent manne1' FITC-Annex.in V staining, DNA fragmentation t esting. and Hoechst 33258 s taining revealed that ES inhibits cell growth via apoptosis. ES bl ocked cell-cycle prog1'ession at t he sub-Gl phase‘ wi th decreased expression of cyclins Dl, D2‘ and E, and their activating partn ers cdk2‘ cdk4‘ and cdkfì, and a concomitant induction of p53 and p21/WAF1. Furthe1'more, ES treatment in creased the cytosolic level of cytochrome c and resulted in caspase- 3 activation‘ and thi s effect was co1'1'elated with Bax up-regulation and Bcl-2 down-1'egulation Taken together‘ these data suggest that ES is a potential chemopreventive and chemotherapeut ic agent fo r oral ca ncer