I continue to enjoy virtually no tingling after the introduction of horsechestnut, several grams a day.
1: Acta Pharmacol Sin. 2004 Jul;25(7):869-75.Links
Effects of sodium beta-aescin on expression of adhesion molecules and migration of neutrophils after middle cerebral artery occlusion in rats.Hu XM, Zhang Y, Zeng FD.
Institute of Clinical Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.
AIM: To investigate the effects of sodium beta-aescin on neutrophil migration and expression of adhesion molecules (ICAM-1 and E-selectin) after middle cerebral artery occlusion (MCAO) in rats. METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO. After a 2-h ischemia and a 24-h reperfusion, the infarct volume and neurological deficit were determined by the method of TTC staining and the Longa's score. The effect of sodium beta-aescin on the migration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO) enzyme. The expressions of adhesion molecules were determined by immunohistochemistry and Western blot. RESULTS: Sodium beta-aescin significantly reduced the cerebral infarct volume and ameliorated the neurological deficit (P<0.05 or P<0.01). The MPO activity and the expressions of ICAM-1 and E-selectin in the vehicle-treated rats were increased significantly (P<0.01) after cerebral I/R. After treatment with sodium beta-aescin, the enzymatic activity of MPO and the expressions of these adhesion molecules were significantly reduced compared with the vehicle-treated group (P<0.05 or P<0.01). CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R.
PMID: 15210059 [PubMed - indexed for MEDLINE]
1: BMC Cardiovasc Disord. 2001;1:5. Epub 2001 Dec 7. Links
Rational therapy of chronic venous insufficiency--chances and limits of the therapeutic use of horse-chestnut seeds extract.Ottillinger B, Greeske K.
bertram.ottillinger@vicron.net
BACKGROUND AND METHODS: We report two clinical studies, one already published, performed in patients with early and advanced chronic venous insufficiency (CVI). In both, compression therapy and oral therapy with horse-chestnut seeds extracts (HCSE) were compared to placebo. RESULTS: The published study in early CVI (Grade I) showed HCSE and compression to be superior to placebo and to be equivalent to each other in reducing lower leg volume, a measure for oedema.In the study, in advanced CVI (Grade II and IIIa), compression appeared to be superior to placebo, whereas HCSE was not. HCSE fared better in Grade II than in Grade IIIa patients.These results are discussed in the light of data from an in vitro model, where HCSE has been able to close the intercellular gaps in the venular endothelium. Not fully specified factors lead to an opening of these gaps, resulting in oedema as well as in local coagulation and thrombosis. The subsequent inflammation keeps these gaps open and initiates and maintains a chronic disease process, which may be the starting point of CVI. CONCLUSION:
Due to its ability to close the venular endothelial gaps, HCSE seems to be a suitable and protecting therapy during the early stages of CVI. In later more severe stages compression therapy is indicated. Taking into account the observed negative impact of compression on quality of life, pharmacological CVI therapy should start early to avoid progress and to spare patients compression therapy.
PMID: 11747472 [PubMed - indexed for MEDLINE]
PMCID: PMC61039
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1: Eur J Pharmacol. 1998 Mar 12;345(1):89-95. Links
Effect of aescine on hypoxia-induced neutrophil adherence to umbilical vein endothelium.Bougelet C, Roland IH, Ninane N, Arnould T, Remacle J, Michiels C.
Laboratoire de Biochimie et Biologie Cellulaire, Facultés Universitaires Notre-Dame de la Paix, Namur, Belgium.
Although venous stasis due to blood stagnation in lower limbs has been recognised as an important etiological factor for the development of varicose veins, the mechanism linking this ischemic situation to the modifications of the venous wall in varicose veins is still unclear. There is evidence that the activation of the endothelium during blood stasis and its subsequent cascade of interactions with other cell types could alter the structure of the vein wall and could possibly be at the origin of the disease. While phlebotonic drugs are often used to improve symptoms in chronic venous insufficiency, their precise mechanism of action is not well understood. We now tested aescine (Reparil i.v. form) in an ex vivo model which mimics this situation, i.e., perfused human umbilical vein exposed to hypoxic conditions. To study the effect of aescine on neutrophil activation and adhesion to the endothelium, human umbilical veins were incubated under hypoxic conditions with or without aescine and the interactions between the endothelium and neutrophil-like cells, HL60, were investigated. We observed that a large number of HL60 became adherent to the endothelium of veins after 2 h hypoxia and that these adherent HL60 were activated: they released high amounts of superoxide anion and of leukotriene B4. Aescine (250 ng/ml or 0.22 microM) was shown to markedly inhibit HL60 adherence to hypoxic endothelium. By decreasing the number of adherent HL60, aescine also decreased the subsequent production of superoxide anion and of leukotriene B4. Scanning electron microscopy confirmed the increased HL60 adherence to the endothelium, as well as the inhibitory effect of aescine. These results support results of in vitro studies on isolated endothelial cells in which aescine was shown to inhibit the hypoxia-induced activation of endothelial cells and the subsequent increased adherence of neutrophils. In vivo, the activated and infiltrated leukocytes release free radicals, chemotactic molecules such as leukotriene B4 and proteases which then can degrade the extracellular matrix. These processes could contribute to alterations of the venous wall similar to those observed in varicose veins. By maintaining an intact endothelium during in vivo blood stasis in the lower limbs and preventing neutrophil recruitment, adherence and activation, aescine could prevent the resulting alterations of the venous wall. These results could explain at least in part the potential benefit of the drug in the prevention of venous insufficiency.
PMID: 9593599 [PubMed - indexed for MEDLINE]
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1: Biol Pharm Bull. 1997 Oct;20(10):1092-5.Links
Effects of escins Ia, Ib, IIa, and IIb from horse chestnut, the seeds of Aesculus hippocastanum L., on acute inflammation in animals.Matsuda H, Li Y, Murakami T, Ninomiya K, Yamahara J, Yoshikawa M.
Kyoto Pharmaceutical University, Japan.
We investigated the effects of escins Ia, Ib, and IIb isolated from horse chestnut, the seeds of Aesculus hippocastanum L., and desacylescins I and II obtained by alkaline hydrolysis of escins on acute inflammation in animals (p.o.). Escins Ia, Ib, IIa, and IIb (50-200 mg/kg) inhibited the increase of vascular permeability induced by both acetic acid in mice and histamine in rats. Escins Ib, IIa, and IIb (50-200 mg/kg) also inhibited that induced by serotonin in rats, but escin Ia didn't. Escins Ia, Ib, IIa, and IIb (200 mg/kg) inhibited the hind paw edema induced by carrageenin at the first phase in rats. Escin Ia (200 mg/kg) and escins Ib, IIa, and IIb (50-200 mg/kg) inhibited the scratching behavior induced by compound 48/80 in mice, but escin Ia was weakest. Desacylescins I and II (200 mg/kg) showed no effect. With regard to the relationship between their chemical structures and activities, the acyl groups in escins were essential. Escins Ib, IIa, and IIb with either the 21-angeloyl group or the 2'-O-xylopyranosyl moiety showed more potent activities than escin Ia which had both the 21-tigloyl group and the 2'-O-glucopyranosyl moiety.
PMID: 9353571 [PubMed - indexed for MEDLINE]
link3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
