ABSTRACT
Sixteen steroidal saponins, including seven previously unreported compounds, were isolated from Tribulus terrestris. The structures of the saponins were established using 1D and 2D NMR spectroscopy, mass spectrometry, and chemical methods. They were identified as: 26-O-ß-d-glucopyranosyl-(25R)-furost-4-en-2α,3ß,22α,26-tetrol-12-one (terrestrinin C), 26-O-ß-d-glucopyranosyl-(25R)-furost-4-en-22α,26-diol-3,12-dione (terrestrinin D), 26-O-ß-d-glucopyranosyl-(25S)-furost-4-en-22α,26-diol-3,6,12-trione (terrestrinin E), 26-O-ß-d-glucopyranosyl-(25R)-5α-furostan-3ß,22α,26-triol-12-one (terrestrinin F), 26-O-ß-d-glucopyranosyl-(25R)-furost-4-en-12ß,22α,26-triol-3-one (terrestrinin G), 26-O-ß-d-glucopyranosyl-(1â6)-ß-d-glucopyranosyl-(25R)-furost-4-en-22α,26-diol-3,12-dione (terrestrinin H), and 24-O-ß-d-glucopyranosyl-(25S)-5α-spirostan-3ß,24ß-diol-12-one-3-O-ß-d-glucopyranosyl-(1â4)-ß-d-galactopyranoside (terrestrinin I). The isolated compounds were evaluated for their platelet aggregation activities. Three of the known saponins exhibited strong effects on the induction of platelet aggregation.
Subject(s)
Drugs, Chinese Herbal/isolation & purification , Phytosterols/isolation & purification , Platelet Activating Factor/isolation & purification , Saponins/isolation & purification , Tribulus/chemistry , Drugs, Chinese Herbal/chemistry , Drugs, Chinese Herbal/pharmacology , Molecular Structure , Nuclear Magnetic Resonance, Biomolecular , Phytosterols/chemistry , Phytosterols/pharmacology , Platelet Activating Factor/chemistry , Platelet Activating Factor/pharmacology , Saponins/chemistry , StereoisomerismABSTRACT
Intestinal bacterial proliferation is an important aspect of gastrointestinal injury in neonatal necrotizing enterocolitis (NEC). In the present investigation, we examined the protective action of oral supplementation with Saccharomyces boulardii (S. boulardii), non-pathogen probiotic yeast, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. Young mice were divided into three groups; Group 1 mice (untreated) were subjected only to hypoxia-reoxygenation; Group 2 mice were subjected to hypoxia-reoxygenation and were then given lyophilized S. boulardii (10 mg suspended in 0.5 ml saline) twice a day by orogastric intubation for 10 days. Group 3 mice served as controls. Hypoxia was induced by placing young mice in a 100 % CO (2) chamber for 5 min. After hypoxia, the young mice were reoxygenated for 10 min with 100 % oxygen. We examined the intestinal lesions by light microscopy and measured intestinal generation of PAF and TNF-alpha in the H/R-induced model of NEC. In the probiotic group, NEC-induced intestinal tissue damage was greatly attenuated, with necrosis partially limited to the mucosa. Both intestinal tissue PAF and TNF-alpha concentrations were significantly higher in the untreated group than in controls (p < 0.001). S. boulardii-supplemented young mice showed a significant decrease in intestinal generation of PAF compared with untreated young mice (p < 0.05). On the other hand, no significant difference was observed in the intestinal concentration of TNF-alpha between untreated and probiotic groups ( p > 0.05). The present study suggests that hypoxia/reoxygenation plays an important role in the pathogenesis of NEC and supports hypothesis that especially PAF and TNF-alpha are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with S. boulardii ameliorates the histologic evidence of H/R-induced intestinal injury. Based on these findings, the beneficial effects of probiotic S. boulardii in this model of NEC are mediated via mechanisms inhibiting intestinal proinflammatory mediator release.
Subject(s)
Enterocolitis, Necrotizing/microbiology , Enterocolitis, Necrotizing/therapy , Saccharomyces/physiology , Animals , Biological Therapy , Enterocolitis, Necrotizing/etiology , Hypoxia/complications , Intestinal Mucosa/microbiology , Intestinal Mucosa/pathology , Mice , Mice, Inbred BALB C , Oxygen , Platelet Activating Factor/isolation & purification , Tumor Necrosis Factor-alpha/isolation & purificationABSTRACT
Lipids from strawberry fruits, leaves, achenes and pollen were separated into classes by TLC, purified by HPLC and tested for biological activity. A lipid fraction from fruits with the same chromatographic behaviour as authentic platelet activating factor (PAF) showed identical biological activity, namely, dose-dependent aggregation of washed rabbit platelets, inhibition of aggregation by CV 3988, platelet desensitization to PAF and vice versa, and loss of activity by alkaline hydrolysis and recovery of activity by reacetylation. The presence of PAF was confirmed by FAB mass spectrometry. Lyso-phosphatidylcholines, including lyso-PAF, were also found in all the plant parts tested.
Subject(s)
Fruit , Lysophosphatidylcholines/isolation & purification , Platelet Activating Factor/isolation & purification , Platelet Activating Factor/pharmacology , Platelet Aggregation/drug effects , Animals , Chromatography, High Pressure Liquid , Chromatography, Thin Layer , In Vitro Techniques , Lysophosphatidylcholines/chemistry , Phospholipid Ethers/pharmacology , Plant Leaves , Platelet Activating Factor/chemistry , Platelet Aggregation Inhibitors/pharmacology , Pollen , Rabbits , Spectrometry, Mass, Fast Atom BombardmentABSTRACT
Experiments showed that intravenous administration of pheretima decoction elicited pronounced decrease of hypotension in rats. Pretreatment with CV6209, a specific PAF antagonist, significantly inhibited the hypotensive activity of pheretima. Furthermore, an analog of PAF was separated from the total lipids of pheretima and its content was measured to be around 90-130 ng/g.