phytosterols and lyoniside

To investigate the chemical constituents from aerial part of Curcuma wenyujin.. Compounds were isolated by repeated column chromatography on silica gel. Their structures were elucidated on the basis of spectral analysis and comparison with literature data.. Six compounds were isolated and identified as codonolactone (1), voleneol (2), octacosanoic acid (3), beta-sitosterol (4), mangdesisterol (5), and daucosterol (6).. Compounds 1, 2, and 5 were isolated from the plant for the first time.

Topics: Curcuma; Fatty Acids; Phytosterols; Plant Components, Aerial; Plants, Medicinal; Sesquiterpenes; Sitosterols

We hypothesized that the phytosterols beta-sitosterol (BSS), beta-sitosterol glucoside (BSSG), and Moducare (MC; BSS:BSSG = 99:1) could modulate the growth of estrogen-dependent human breast cancer cells in vitro and in vivo. The present study evaluated the estrogenic and antiestrogenic effects of BSS, BSSG, and MC (0.001 to 150 micromol/L) on the proliferation of Michigan Cancer Foundation 7 (MCF-7) cells in vitro. Both BSS (>1 micromol/L) and MC (>50 micromol/L) increased MCF-7 cell proliferation. Treatment with 150 micro mol/L of BSS and MC increased cell growth by 2.4 and 1.5 times, respectively, compared to the negative control (NC) group. However, BSSG had no effect at the concentrations tested. The effects of dietary BSS, BSSG, and MC on the growth of MCF-7 cells implanted in ovariectomized athymic mice were also evaluated. Estrogenic effects of the phytosterols were evaluated in the NC, BSS, BSSG, and MC treatment groups, and antiestrogenic effects were evaluated in the 17 beta-estradiol (E(2)), E(2) + BSS, E(2) + BSSG, and E(2) + MC treatment groups. Mice were treated with dietary BSS (9.8 g/kg AIN93G diet), BSSG (0.2 g/kg diet), or MC (10.0 g/kg diet) for 11 wk. Dietary BSS, BSSG, and MC did not stimulate MCF-7 tumor growth. However, dietary BSS, BSSG, and MC reduced E(2)-induced MCF-7 tumor growth by 38.9% (P < 0.05), 31.6% (P = 0.08), and 42.13% (P < 0.05), respectively. The dietary phytosterols lowered serum E(2) levels by 35.1, 30.2, and 36.5% in the E(2) + BSS, E(2) + BSSG, and E(2) + MC groups, respectively (P < 0.05), compared to that of the E(2) treatment group. Estrogen-responsive pS2 mRNA expression in tumors did not differ among groups, but expression of the antiapoptotic marker B-cell lymphoma/leukemia-2 (bcl-2) in tumors from the E(2) + MC group was downregulated, compared to that of the E(2) treatment group. In summary, BSS and MC stimulated MCF-7 cell growth in vitro. Although BSSG comprises only 1% of MC, BSSG made MC less estrogenic than BSS alone in vitro. However, dietary BSS and MC protected against E(2)-stimulated MCF-7 tumor growth and lowered circulating E(2) levels.

Topics: Animals; Breast Neoplasms; Cell Division; Cell Line, Tumor; Drug Combinations; Drug Implants; Estradiol; Estrogen Antagonists; Female; Humans; Mammary Neoplasms, Experimental; Membrane Proteins; Mice; Mice, Nude; Neoplasm Transplantation; Organ Size; Ovariectomy; Phytosterols; Presenilin-2; Proto-Oncogene Proteins c-bcl-2; Sitosterols; Uterus

The factors responsible for ALS-parkinsonism dementia complex (ALS-PDC), the unique neurological disorder of Guam, remain unresolved, but identification of causal factors could lead to clues for related neurodegenerative disorders elsewhere. Earlier studies focused on the consumption and toxicity of the seed of Cycas circinalis, a traditional staple of the indigenous diet, but found no convincing evidence for toxin-linked neurodegeneration. We have reassessed the issue in a series of in vitro bioassays designed to isolate non-water soluble compounds from washed cycad flour and have identified three sterol beta-d-glucosides as potential neurotoxins. These compounds give depolarizing field potentials in cortical slices, induce alterations in the activity of specific protein kinases, and cause release of glutamate. They are also highly toxic, leading to release of lactate dehydrogenase (LDH). Theaglycone form, however, is non-toxic. NMDA receptor antagonists block the actions of the sterol glucosides, but do not compete for binding to the NMDA receptor. The most probable mechanism leading to cell death may involve glutamate neuro/excitotoxicity. Mice fed cycad seed flour containing the isolated sterol glucosides show behavioral and neuropathological outcomes, including increased TdT-mediated biotin-dUTP nick-end labelling (TUNEL) positivity in various CNS regions. Astrocytes in culture showed increased caspase-3 labeling after exposure to sterol glucosides. The present results support the hypothesis that cycad consumption may be an important factor in the etiology of ALS-PDC and further suggest that some sterol glucosides may be involved in other neurodegenerative disorders.

Topics: Amyotrophic Lateral Sclerosis; Animals; Astrocytes; Biological Assay; Cells, Cultured; Cerebral Cortex; Cholesterol; Cycas; Dementia; Glucose; Glucosides; Guam; Humans; In Vitro Techniques; Male; Mice; Neurons; Neurotoxins; Parkinsonian Disorders; Patch-Clamp Techniques; Phytosterols; Plant Extracts; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Seeds; Sitosterols; Stigmasterol

Topics: Cellulose; Phytosterols; Sitosterols; Uridine Diphosphate Glucose