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It has been established in experiments on 73 rabbits that ascorbic acid inhibits the development of hypercholesterinemia, peroxidation syndrome and atherosclerotic affection of the aortas. Rutin delays the development of hypercholesterinemia and peroxidation syndrome and tends to inhibiting aortal atherosclerotic affection.
In Wistar rats, combined treatment with ethanol or carbon tetrachloride and a mixture of coumarin and sodium salt of rutin sulphate (Venalot injectable solution) causes slight increases of some liver-specific enzymes in plasma. This effect was not observed in DBA/2 4-mice whose metabolism of coumarin is widely analogous to that of man. The LD50 for coumarin in those mice was twice that in rats. These results are discussed in the light of different metabolic pathways of coumartin in both species.
The effect of Venalot, a combination of coumarin and rutin sulphate, on stimulated exocrine secretion of the pancreas and on changes of pancreatic enzymes in thoracic duct lymph was studied in 10 subjects with normal function of the pancreas. Venalot has no direct effect on the exocrine function of the pancreas. Following administration of the compound, the amylase and lipase activity in thoracic duct lymph increases temporarily, probably as a consequence of outflow from the interstitial liquid of the pancreas.
The agonistic actions of angiotensin II and prostaglandin E2 (PGE2) were plotted on the guinea-pig ileum as cumulative dose-response curves. The same actions were also studied in the presence of vitamin K3,, streptomycin and rutin which antagonized each of the agonists non-competitively. By comparison of the affinity constants of antagonists, it was determined that the antagonism occurs by a common mechanism.
A rapid and specific reversed-phase high performance liquid chromatography (RP-HPLC) method with diode array detection (DAD) at room temperature was used and validated for the simultaneous determination of five flavonoids (catechin, CA; rutin, RU; quercetin, QU; kaempferol, KA; isorhamnetin, IS) in the extract of sea buckthorn (Hippophae rhamnoides L.) leaves. The sample pretreatment process involved ultrasonic extraction with 85% ethanol under the frequency of 80 kHz, at a temperature of 45 degrees C for 30 min and with the ratio of liquor to material of 15 mL g-1, followed by separation on HIQ SIL C18V column with methanol-acetonitrile-water (40:15:45, v/v/v) containing 1.0% acetic acid as a mobile phase. The extract was detected by DAD at the wavelength of 279 nm for CA, 257 nm for RU, 368 nm for QU, KA and IS. Calibration curves were found to be linear with the ranges of 0.011-0.520 mg ml-1 (CA), 0.007-0.500 mg ml-1 (RU), 0.019-0.280 mg ml-1 (QU), 0.010-0.440 mg ml-1 (KA) and 0.008-0.400 mg ml-1 (IS). The correlation coefficients of linear regression analysis and detection limits were between 0.9963-0.9999 and 0.00079-0.00290 mg ml-1. The contents of CA, RU, QU, KA and IS in sea buckthorn leaves were successfully determined with 3.8, 5.2, 7.3, 10.9 and 11.9 min with satisfactory reproducibility and recovery. Recoveries of the five flavonoids were between 97.27 and 99.98%. The method was applied to the determination of flavonoids in sea buckthorn leaves and was found to be simple, rapid and efficient.
The dietary effect of monoglucosyl-rutin (M-R), a flavonoid, on azoxymethane (AOM)-induced colon carcinogenesis was investigated in two experiments with 5 week old, F344 male rats. In the first experiment (5 weeks study), effects of MR on AOM (15 mg/kg body weight 3 times weekly)-induced formation of aberrant crypt foci (ACF) in five groups were assessed. In this experiment, group 3 given 500 ppm M-R with AOM had a significantly smaller number of ACF containing 4 or more aberrant crypts than group 1 with AOM alone, and groups 2 and 3 given 100 ppm or 500 ppm M-R respectively had significantly lower BrdU labeling indices in the epithelial cells of large bowel than group 1. For the second experiment, rats were divided into 8 groups. Groups 1-5 were given AOM as in the first experiment. Groups 2-5 were fed diets containing 100ppm or 500ppm M-R for 4 weeks in the initiation phase or 36 weeks in the post-initiation phase. Group 6 was given 500ppm M-R throughout the experiment, and group 7 was kept on the basal diet and served as a control. At the termination of the experiment (40 weeks after the start), groups 2-5 had significantly smaller numbers of positive cells with anti-proliferating cell nuclea antigen (PCNA) antibody than group 1. Furthermore, group 5 treated with 500ppm M-R for 36 weeks demonstrated tendencies for decrease in the incidence and multiplicity of colon tumors. These data suggest that M-R has the potential to inhibit AOM-induced colon carcinogenesis.
An experimental investigation was made of the influence of 0-(beta-hydroxyethyl)-rutin (HR) on the effect of indomethacin (1, 2 or 4 mg/kg i.p.) in inhibiting rat paw oedema. HR was given once daily during a 6-day pretreatment, with the final dose 90 minutes before the inflammatory reaction was induced. In the group of HR-pretreated rats which also received indomethacin in a dose of 2 or 4 mg/kg, the extent of the carrageenin-oedema was diminished significantly in comparison to that in experimental animals treated merely with indomethacin.
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