aesculus hippocastanum/항진균제

β-escin is a mixture of triterpene saponins isolated from the horse chestnut seeds (Aesculus hippocastanum L.). The anti-edematous, anti-inflammatory and venotonic properties of β-escin have been the most extensively clinically investigated effects of this plant-based drug and randomized controlled

A new prenylated coumarin, S-6-[2-(hydroxymethyl)butoxy]-7-hydroxy-4-methyl-2 H-chromen-2-one ( 1), named pavietin, has been isolated from the leaves of an Aesculus pavia genotype along with three known flavonol glycosides, quercetin 3- O-alpha-rhamnoside (quercitrin, 2), quercetin 3-

Aescin, the major active principle from Aesculus hippocastanum (Hippocastanaceae) the horse chestnut tree, has shown satisfactory evidence for a clinically significant activity in chronic venous insufficiency (CVI), haemorrhoids and post-operative oedema. In one controlled trial aescin was shown to

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

Although Bell's palsy is the most common acute facial paralysis, the cause of it is still unknown. This made the treatment for it remain very limited. Many methods are simply symptomatic treatment. Up to now we have known that Bell's palsy is related to viral infection and the pathomechanism of

Impairment of the cutaneous microcirculation is a major predisposing factor in inflammation and ulceration in patients with chronic venous insufficiency (CVI). Increase of capillary filtration rate predisposes to the formation of edema. Local lymphedema is a complication of CVI, often

Adenosine diphosphate (ADP) plays a pivotal role in platelet activation. Platelet hyperactivity is associated with vascular disease and also has a key role in haemostasis and thrombosis. ADP activates platelets through three purinoceptor subtypes, the G(q)-coupled P2Y(1) receptor, G(i)-coupled