Rutoside Research Articles

Physico-Chemical and Pharmaco-Technical Characterization of Inclusion Complexes Formed by Rutoside with β-Cyclodextrin and Hydroxypropyl-β-Cyclodextrin Used to Develop Solid Dosage Forms

The aim of our study was to obtain rutoside (RUT) inclusion complexes in β-cyclodextrin (β-CD) and in hydroxypropyl-β-cyclodextrin (HP-β-CD), in a 1:1 molar ratio, using the lyophilization method of complexation in solution. The complexes were confirmed and characterized, in comparison with the raw materials and their simple physical mixtures, by SEM, DSC, and FT-IR analyses. The antioxidant activity of the compounds was assessed by using the 2,2-diphenyl-1-picryl-hydrazyl (DPPH) and 2’-azino-bis(3-ethylbenzothiazolin-6-sulfonic) acid (ABTS) radicals, determining the radical scavenging activity, and by ferric reducing antioxidant power (FRAP) assay. The results revealed superior antioxidant ability for the inclusion complexes towards rutoside alone. The inclusion complexes were used as active ingredients in formulations of immediate-release tablets. The preformulation studies were performed on the powders for direct compression obtained after mixing the active ingredients with the excipients (Avicel PH 102, Polyplasdone XL-10, magnesium stearate, and talc). The materials were assessed for particle size, flowability, compressibility, and moisture content, establishing they are suitable for a direct compression process. The tablets were characterized regarding their pharmaco-technical properties and the results proved that the formulations lead to high-quality delivery systems, showing a good mechanical resistance with a low friability, excellent disintegration times, and satisfying dissolution rate. The performances were very similar for both formulations and the physico-mechanical properties of the tablets are not influenced by type of the used cyclodextrin, but the RUT- HP-β-CD tablets presented a higher dissolution rate.

Study on vasodilatation effects of total flavonoid from polygonum aviculare on blood vessel of rat in vitro

Objective To investigate the vasodilatation effects of total flavonoid from polygonum aviculare on rat thoracic aorta and its underlying mechanisms. Methods Total flavonoid from polygonum aviculare was gotten by extracted with 65% alcohol, gathered with polyamide, and eluted with 75% alcohol. The content of flavone was determined with rutoside as standard preparation. Normal rats thoracic aorta in vitro used as sample, BL-420E biological functional experiment system was utilized to record dilatation effect of total flavonoid on PE affecting pre-contracting blood vessel and the relation between dilatation effect of total flavonoid on blood vessel and calcium influx. Results Total flavonoids from polygonum aviculare can diastole contractions of thoracic aorta caused by PE. In calcium-free perfusion, gradually adding CaCl2 induced calcium influx. Clinical data showed dose-effect relation between drug and blood vessel contraction decreased in the total flavonoids from polygonum aviculare incubation rats than normal rats. Besides, total flavonoids from polygonum aviculare can obviously inhibit contraction of blood vascular circle induced by calcium releasing. Conclusion FP exerted a dose-dependent vasodilatation effect on rat isolated aorta rings by inhibiting Ca2＋ influx via L-type voltage-gated Ca2＋ channels and Ca2＋ release from sarcoplasmic reticulum, consequently decrease Ca2＋ in vascular smooth muscle cells. Key words: Polygonum aviculare; Total flavone; Hypertension; Vasodilation

Hemathidrosis: a case report.

A 15-year-old male patient presented with intermittent red secretion on the face, upper limbs, nail grooves, fingers and toes for more than 10 months. Ten months prior to the presentation, red secre-tions began to emerge on the face, especially ears, eyes and the surrounding area of nose, following a severe psychical stimulus. The attack typically lasted 2-3 minutes before spontaneous stop with the formation of blood crusts. The frequency was 1-4 per day during the attack of hemathidrosis which might last 1 week. The interval was irregular and varied from 10 days to months. There was no blood stasis, bruise or wound left on the skin after the wipe of bloodstain, and no itch or pain was complained of. Before the secretion of bloody sweat, the patient was always fidgety, irritable, and sometimes excited or difficult to sleep, but the secretion never occurred at night. After several episodes, bloody sweat also appeared in succession and symmetrically on the forearms, extensor crura, fingers, toes and perionychium. The cell components of bloody sweat were identical to those of peripheral blood. The patient was diagnosed as hemathidrosis. No abnormality was found in labora-tory tests, histopathological examination, electron microscopy or radiology. No relief of symptoms was achieved after treatment with vitamin C, rutoside and oryzanol. Hemathidrosis is a rare disease, and to clarify its patho-genesis is essential for its treatment. Key words: Hemathidrosis; Pathology; Microscopy; electron

Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis

BackgroundDietary flavonols may play an important role in the adjunct therapy of chronic inflammation. The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model.MethodsRU was added simultaneously to human macrophages during their activation. Cells were then analyzed for inflammation-related gene expression using a specific array, and cell supernatants were collected to measure inflammatory mediators. RU was also injected into adjuvant-induced arthritic rats, and disease progression and body weight were evaluated until 50 days after injection. Sera and peritoneal macrophages were also collected to quantify the RU effect on various inflammatory markers.ResultsRU inhibited inflammation-related gene expression in activated human macrophages and the release of nitric oxide, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 from these cells. In a rat model, RU inhibited clinical signs of chronic arthritis, correlating with decreased levels of inflammatory cytokines detected in rat sera and macrophage supernatants.ConclusionThus, RU may have clinical value in reducing inflammatory manifestations in human arthritis and other inflammatory diseases.