Mediation of the cytotoxicity of lanostanoids and steroids of Ganoderma tsugae through apoptosis and cell cycle.

A new lanostanoid ester glucoside, 3 alpha-acetoxy-5 alpha-lanosta-8,24-dien-21-oic acid ester beta-d-glucoside (1), and a known steroid, 2 beta,3 alpha,9 alpha-trihydroxy-5 alpha-ergosta-7,22-diene (2), were isolated from the fruit bodies of Ganoderma tsugae and their structures determined by spectroscopic methods. To study the cytotoxicity of 1 and 2, the changes of DNA content in human hepatocytes (Hep 3B) were studied. A sub-G1 cell stage was drastically increased after 24-h incubation with 1 (24 micrograms/mL). Compound 2 (100 micrograms/mL) inhibited the cell cycle progression of Hep 3B cells at the G2/M phase with an IC50 value of about 87.1 micrograms/mL. These results indicate that 1 causes cell death by apoptosis and 2 may possess the activity of cell cycle inhibition.

Benzoquinones, a homoisoflavanone and other constitutents from Polygonatum alte-lobatum.

From the rhizomes of Polygonatum alte-lobatum, two new homologous series of 1,4-benzoquinones, polygonaquinones A and B, a novel homoisoflavanone, a new gentrogenin glycoside and 13 known compounds were isolated and characterized. The structures of the new compounds were determined as two homologous series of three 2,5-dihydroxy-3-methyl-6-alkyl-1,4-benzoquinones and three 2-hydroxy-3-methyl-6-alkyl-1,4-benzoquinones, with chain lengths C21 to C23, and 4',5,7-trihydroxy-6,8-dimethylhomoisoflavanone and gentrogenin 3-O-beta-D-glucopyranosyl(1-->2)-[beta-D-xylopyranosyl(1-->3)] -beta-D-glucopyranosyl(1-->4)-beta-D-galactopyranoside.

Comparison of a high lipase pancreatic enzyme extract with a regular pancreatin preparation in adult cystic fibrosis patients.

BACKGROUND: Malabsorption due to exocrine pancreatic insufficiency is the main gastrointestinal problem in cystic fibrosis. Despite high doses of pancreatic enzyme supplements it is often not possible to normalize fat absorption. We compared a new high lipase pancreatic enzyme preparation (Pancrease-HL; Cilag, Brussels, Belgium), containing enteric coated microspheres with 25,000 U of lipase, 22,500 U of amylase and 1250 U of protease per capsule, with regular Pancrease capsules, containing 5000 U of lipase, 2900 U of amylase and 330 U of protease per capsule. METHODS: In a randomized double-blind crossover study, 13 cystic-fibrosis patients (6 male, 7 female, mean age 27.7 years) received either four capsules of Pancrease t.d.s. or one capsule of Pancrease-HL t.d.s. Patients took 20 mg omeprazole daily to raise intra-duodenal pH and thus optimize release of enzymes from the enteric coated microspheres. RESULTS: With four capsules of Pancrease t.d.s., mean fat excretion was 15.4% and mean nitrogen excretion was 19.9% vs. 15.5% fat and 19.9% nitrogen excretion with one capsule Pancrease-HL t.d.s. Fat and protein energy loss (as a percentage of total daily intake) was 18.3% with Pancrease and 18.2% with Pancrease-HL. The differences were not statistically significant. Pancrease-HL was well tolerated, with no difference in abdominal pain or general well-being scores. The number and average weight of stools passed remained the same. CONCLUSIONS: One capsule of Pancrease-HL appears to be equivalent to four capsules of regular Pancrease. Treatment with less capsules per day with the same efficacy may facilitate patient compliance.

Antiplatelet effects and vasorelaxing action of some constituents of Formosan plants.

Various xanthones as well as quercetin have been shown to exhibit antiplatelet activity. A series of anthraquinones analogues structurally related to xanthones and a series of quercetin-related compounds were tested for their antiplatelet effects. Emodin, frangulin B, kaempferol tetraacetate, quercetin-3-O-galactoside octaacetate, rhamnazin triacetate, and rhamnetin tetraacetate were found to be potent antiplatelet agents, and 1,8-dihydroxy-6-methoxy-3-methylanthraquinone 8-O-rhamnosyl-(1-->2)-glucoside, rhamnustrioside undecaacetate, rutin decaacetate, and quercetin-3-O-(6-O-alpha-L-arabinopyranosyl)-beta-D-galactopyranos ide decaacetate showed significant antiplatelet effects. Quercetin showed vasorelaxing action in rat thoracic aorta.

Cytotoxic principles and their derivatives of Formosan Solanum plants.

The new steroidal alkaloid capsimine-3-O-beta-D-glucoside [1] was isolated from the root bark of Solanum capsicastrum, and carpesterol [2], 3 beta-(p-hydroxy)-benzoyloxy-22 alpha-hydroxy-4 alpha-methyl-5 alpha-stigmast-7-en-6-one [3], and a new steroidal glycoside named indioside A [4] were isolated from the fruit of Solanum indicum. Indioside A was characterized as 3 beta-O-[alpha-L-rhamnopyranosyl-(1-->2), beta-D-glucopyranosyl-(1-->4), beta-D-glucopyranosyl-(1-->3)-]alpha-L-rhamnopyranosyl-(-->2)]-beta-D- glucopyranosyl]-diosgenin. Khasianine, dihydrosolasodine, capsimine, and capsimine-3-O-beta-D-glucoside exhibited strong activity against liver damage induced by CCl4. Capsimine and narigenin exhibited significant cytotoxic effect against human PLC/PRF/5 and KB cells in vitro, and capsicastrine and etioline exhibited significant cytotoxicity against human PLC/PRF/5 cells in vitro.

Flavonol and anthraquinone glycosides from Rhamnus formosana.

Two new flavonol triglycosides, and a new anthraquinone glycoside, have been isolated from the roots of Rhamnus formosana. These compounds have been characterized as rhamnazin 3-O-[alpha-L-rhamopyranosyl(1----4)-alpha-L-rhamnopyranosyl(1----6 )]-beta-D-galactopyranoside (rhamnazin 3-isorhamninoside), rhamnocitrin 3-O-isorhamninoside and 1,6,8-trihydroxy-3-methylanthraquinone 1-O-rhamnosyl(1----2)glucoside, respectively.

Antihepatotoxic principles of Solanum capsicastrum.

Two new steroidal alkaloids named capsimine and isocapsicastrine were isolated from the root bark of Solanum capsicastrum. Their structures were elucidated by chemical degradation and spectral data as (22R, 25R)-22,26-epiminocholest-5-ene-3 beta, 16 alpha-diol and (22S,25S)-O(3)-beta-D-glucopyranosyl-22,26-epiminocholest-5-ene-3 beta-16 alpha-diol, respectively. Capsicastrine, capsicastrine acetate, isoteinemine acetate, and etioline exhibited strong activity against liver damage induced by CCl4.