PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Escin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1976

[On the pharmacodynamics of alpha- and beta-escin after oral application (author's transl)].

Contrary to the almost water insoluble crystalline beta-escinic acid, the water soluble forms of escin -- such as alpha-escinic acid or its salts, Na-b-escinate and the amorphous beta-escinic acid -- are so well absorbed by the gastro-intestinal tract that the effects after oral application could be compared with those of the reference substances furosemide, hydrocortisone, acetylsalicylic acid, azapropazone and phenylbutazone. Escin was tested in the stasis edema, cotton-pellet-granuloma, and UV-erythema, i.e., in test models which seem specially suited to characterize the properties of this substance. In these tests which reflect both the prophylactic and the therapeutic treatment escin has proven antiexudative-antiphlogistic effects. They are based on a favorable influence of permeability and diuresis.

Animals↗
PubMed1979

Venotonic activity of escin on the human saphenous vein.

The venotonic effects of escin on the human saphenous vein have been evaluated in vitro on histologically normal venous segments obtained during surgical saphenectomy procedures. It is necessary to use the human preparations because of the great variability in the responses of the veins of different species. By using a standard stimulus and fitting the experimental data to the logistic function, we were able to compare the activity of escin with those of the commonly used venotonic agents. Stimulation with escin always induced an increase in venous tone which was constant for a given dose and stable for some time, and maintained for as long as an hour after removal of the substance from the bath. The maximum contraction obtained with escin was similar to those obtained with serotonin and dihydroergotamine, significantly greater than that obtained with acetylcholine or vasopressin. However, the affinity of escin was found to be lower than those of the other substances studied. An increase in venous tone, and therefore a decrease in the volume of the venous district, would be considered a very favorable result to be obtained with a drug which, like escin, is indicated for treatment of venous diseases leading to irreversible dilation.

Escin↗
PubMed1977

[Thermometric investigations about the efficacy of beta-escin to reduce postoperative edema (author's transl)].

Beta-escin is highly effective in reducing postoperative edemas and swellings. It was tried to demonstrate the effect of beta-escin using the thermometry. The temperature of soft tissues and bones can be measured with the help of the thermometry, in this way the circulation of the skin can be determined. In 65 test persons so-called normal thermograms were established, using the infraredthermometer KT 41, which makes registrations without touching the skin. In 53 patients the temperature of the skin was checked after surgery of the hand. 27 patients received beta-escin (Reparil); 26 patients without medication served as controls. In every case the temperature of the operated hand was compared to the other hand. Among the patients, who received escin, the temperature of the operated hand rose for two days following surgery; afterwards it fell quickly. Among the controls the skin-temperature rose up to the 4. day after surgery and decreased slowly. These results demonstrate clearly that after using beta-escin there is a quick reduction of postoperative inflammation and edema.

Adult↗
PubMed1976

[New findings on the efficacy and mode of action of the horse chestnut saponin escin].

In order to complete previous results of the efficacy of the horse chestnut saponin escin, its activity was tested on two further models of inflammation: the rat serous peritonitis provoked by i.p. injection of formalin solution, and the rat serous pleurisy provoked by intrapleural injection of Evans Blue/carrageenan. The results showed escin to be an anti-exudative substance with regard to its exudation inhibitory effect determined by the reduction of exudative fluid. As to peritonitis the diminution of protein permeation into the abdominal cavity was determined: with increasing doses escin tended to prevent more efficiently the diffusion of small molecules than the permeation of large molecules. The hypothesis that escin has an effect on the vascular walls in the sense of a "sealing" effect on the capillaries was tested on the following model: the permeability of the plasma-lymph barrier of the hind leg of the rabbit was enhanced by injection of bradykinin. Escin antagonised the bradykinin effect dose-dependently determined by the depression of the raised lymph-flow by about 70%.

Animals↗
PubMed1977

[Studies on toxicity and fertility of escin in the rat (author's transl)].

The DL50 of escin was determined after i.p. application. Juvenile male rats were treated with 2X5 mg/kg escin at age 32 days. After they had reached fertility, kidneys, testes and sperm were examined. The high dose of escin used did not affect fertility and a nephrotoxic activity could not be detected either.

Age Factors↗
PubMed1992

Ca-dependent K channels in smooth muscle cells permeabilized by beta-escin recorded using the cell-attached patch-clamp technique.

Using the cell-attached patch-clamp technique, the activity of single, Ca-dependent K channels was recorded in single smooth muscle cells permeabilized by beta-escin. The conductance and the relationship between the open probability of the channels and pCa recorded in permeabilized cells were very similar to those obtained in excised inside-out patches. At pCa 7, application of 30 microM acetylcholine (ACh) or 0.1 microM substance P (SP) together with 1 mM guanosine 5'-trisphosphate to permeabilized cells elicited transient bursts of channel openings similar to those which occur in intact cells. Transient activation was also observed when 2-30 microM inositol trisphosphate (IP3) was applied to permeabilized cells. This single channel activity was inhibited by pretreatment with low-molecular-weight heparin at 50-100 micrograms/ml. Channel activity at pCa 7.0 was greatly enhanced by 200 microM cyclic adenosine monophosphate. These results provide direct evidence that single Ca-dependent K channel activity is regulated by the transmitters ACh and SP, as well as a second messenger, IP3, via the release of intracellular Ca from intracellular sites which are blocked by heparin. This novel approach is valuable in elucidating second messenger mechanisms involved in the regulation of single channel activity by transmitters and autocoids, since permeabilization by beta-escin preserves the entire system of receptor-operated signal transduction and allows intracellular application of second messengers at fixed concentrations.

Acetylcholine↗
PubMedDate not supplied

Histamine release from beta-escin-permeabilized rat peritoneal mast cells and its inhibition by intracellular Ca2+ blockers, calmodulin inhibitors and cAMP.

In order to study the intracellular events leading to histamine release, rat peritoneal mast cells were permeabilized using beta-escin, a triterpenoid. IP3 (0.5-10 microM) dose-dependently elicited significant histamine release from permeabilized mast cells in a Ca2+-free medium, as did GTP-gamma-S at concentrations higher than 5 microM, GTP-gamma-S induced IP3 production dose-dependently in association with histamine release. Histamine release induced by IP3 and GTP-gamma-S was inhibited by pretreatment with TMB-8, while neomycin pretreatment suppressed histamine release caused by GTP-gamma-S but not that caused by IP3.IP3 may cause Ca2+ release from the intracellular Ca2+ store as the key event leading to histamine release. At concentrations higher than 0.1 microM, Ca2+ dose-dependently induced histamine release. Both IP3-and Ca2+-induced histamine release from permeabilized mast cells was inhibited by pretreatment with calmodulin inhibitors (W-7 and calmidazolium), or with cytochalasin D or colchicine. Pretreatment with cAMP also inhibited the histamine release induced by either IP3 or Ca2+. From the present study, it can be assumed that (1) Ca2+ may act on a calmodulin-associated process(es) and cytoskeletal systems, in the process leading to histamine release, and (2) cAMP seems to inhibit histamine release, even in the stages following Ca2+ release from the intracellular Ca2+ store.

Animals↗
PubMed1991

Effects of pinacidil on contractile proteins in high K(+)-treated intact, and in beta-escin-treated skinned smooth muscle of the rabbit mesenteric artery.

1. The effects of pinacidil were investigated on changes in cellular Ca2+ concentration ([Ca2+]i) and tension in intact and chemically skinned smooth muscle strips of the rabbit mesenteric artery. 2. High K+ (128 mM) produced a large phasic followed by a tonic increase in [Ca2+]i and tension in intact muscle strips. Pinacidil at 10 microM but not 1 microM, inhibited the phasic and tonic contractions induced by 128 mM K+ without a corresponding change in [Ca2+]i. 3. In beta-escin-treated skinned smooth muscle, the minimum Ca2+ concentration that produced contraction was 0.1 microM and the maximum contraction was obtained at 10 microM. Pinacidil at 10 microM but not 1 microM, shifted the pCa-tension relation curve to the right and also inhibited the maximum contraction induced by Ca2+. The concentrations of Ca2+ required for half maximal tension were 0.9 microM in control and 1.5 microM in the presence of 10 microM pinacidil. Calmodulin (2 microM) increased the contraction induced by 0.3 microM Ca2+ (but not by 10 microM Ca2+) in the skinned strips. Pinacidil (10 microM) inhibited the contraction induced by 0.3 microM or 10 microM Ca2+ in the presence of 2 microM calmodulin. 4. Noradrenaline (NA, 10 microM) with guanosine triphosphate (GTP, 3 microM), guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S, 3 microM) or 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM) all enhanced the contraction induced by 0.3 microM Ca2+. Pinacidil (10 microM) inhibited the contraction induced by 0.3 microM Ca2+ more strongly in the presence of the above agents than in their absence. 5. Following application of 2 mm adenosine-5'-O-(3-thiotriphosphate) (ATPyS) with 0.3 microM Ca2", 4mM MgATP produced contraction in skinned strips in Ca2 -free solution containing 4mM EGTA ('Ca2+- independent contraction'). The amplitude of the Ca2 +-independent contraction was almost the same as that obtained with 1O microM Ca2 . Pinacidil (1O microM) had no effect on the amplitude of the Ca2+-independent contraction nor did it have any effect on the contraction induced by a solution containing no MgATP ('rigor contraction'). 6. It is concluded that pinacidil (10 microM) acts directly on the contractile apparatus to inhibit Ca2'-induced contraction in smooth muscle of the rabbit mesenteric artery. The site of action of pinacidil may be between Ca2 +-calmodulin complex formation and phosphorylation of the myosin light chain.

Animals↗
PubMed1992

Ca(2+)-induced translocation of protein kinase C during Ca(2+)-dependent histamine release from beta-escin-permeabilized rat mast cells.

When rat mast cells were cultured for a short period in plastic dishes and adhering cells were permeabilized with beta-escin and exposed to Ca2+ at concentrations higher than 10(-7) mol/l, histamine release was induced dose-dependently. Protein kinase C (PKC) activity in the crude extracts obtained from adhering mast cells was induced in the presence of Ca2+, phospholipid and diacylglycerol. The apparent Km value of PKC for Ca2+ was 0.33 mumol/l, and this Ca2+ concentration was equivalent to that which can elicit half the maximum of the Ca(2+0-induced histamine release. After permeabilization, approximately 80% of the total PKC activity remained in the cytosolic fraction. In the resting state, 95% of the total PKC activity was detected in the soluble fraction, and the rest was detected in the membrane fraction. When permeabilized mast cells were incubated with Ca2+ at micromolar concentrations, which are effective in releasing histamine, the total PKC activity did not change. However, the translocation of PKC took place from the cytosolic fraction to the membrane fraction, corresponding to Ca2+ concentrations in the medium. When the crude PKC extract of mast cells was incubated with phospholipid vesicles and centrifuged, the PKC activity in the supernatant was diminished; the amount of PKC binding to the vesicles was dependent upon Ca2+ concentrations in the medium. Calphostin C, a potent PKC inhibitor, interacts with PKC in a noncompetitive manner, and it does not inhibit Ca(2+)-induced translocation of PKC. It can be concluded that PKC is translocated into the cell membrane along with an increase in intracellular Ca2+ concentrations and the subsequent activation of PKC may be crucial for the process leading to histamine release.

Animals↗