What are the internal contents of a chestnut called? Common horse chestnut

It grows naturally in the Balkans. Grows in deciduous forests of the foothills. Photophilous mesophyte, mesotroph. Widely distributed in urban landscaping in Europe, Central Asia, East Asia and North America.

Photo by Elena Bayrasheva

A mighty tree up to 30 m tall with a massive trunk and a heavy, dense, wide-rounded crown, remarkable large inflorescences and very decorative fruits. It deservedly enjoys the reputation of one of the most beautiful park trees, decorative throughout the year: in winter - with a beautiful pattern of powerful branches; in the spring - early blooming, large, sticky, greenish-pink buds, from which on one of the warm days original, wrinkled, complex, long-petioled leaves appear, giving a dense shadow when fully developed. The leaves are compound, palmate, with 5-7 oblong, obovate leaflets up to 25 cm long. In early May, after the leaves bloom, large (up to 30 cm), pyramidal panicles of large, white, pink-speckled flowers appear. Like candles on a Christmas tree, the inflorescences give the tree a unique appearance during this period. Flowering lasts 15-25 days. Chestnut fruits are also very decorative - spherical, green, with numerous thorns, fleshy capsules up to 6 cm in diameter, cracking with three leaves and containing 1-3 shiny, dark brown seeds.

Frost-resistant, quite demanding on soil fertility, prefers loam containing lime. Shade-tolerant, but better development reaches on open sunny places. It is demanding on soil and air moisture, tolerates urban conditions relatively well, and has a high ability to accumulate sulfur compounds and lead. Resistant to pests and diseases. Retains decorative properties for a long time. Very colorful in autumn when the foliage turns a beautiful bright yellow. A good honey plant. Durable.

A first-class tree for planting on streets, boulevards, and park alleys. It is also good for monumental groups and entire groves in large parks and forest parks. Very beautiful in a single planting, where the crown has the opportunity to fully develop. In culture since 1576.

In GBS since 1941, 5 samples (22 copies) were grown from seeds obtained from various botanical gardens. At 61 years old, the height is 13 m, the trunk diameter is 23 cm. It grows from the third ten days of April to the second ten days of October. It grows slowly. It blooms from 9 years old, from the third ten days of May to the second ten days of June. It bears fruit from the age of 9, the fruits ripen in the second half of September. Winter hardiness is high. Seed viability is 100%, germination is average. Reproduction by grafting is possible. Recommended for landscaping in Moscow for alley, group and single plantings.

When storing seeds, it is necessary to maintain humidity (about 40%) and temperature 0 - 5 °C. Before sowing, stratify the seeds in sand at temperatures up to 10 ° C for 2 - 5 months (depending on storage conditions). Usually the seeds are sown no later than next spring after harvest. Sowing depth 6 - 10 cm.

Photo by Olga Blokhman

It has a number of decorative forms: Bauman(f. Baumanii) - with double white flowers and long flowering, does not produce fruit; Schirnhofera (f. Schimhoferi) - with double yellowish-red flowers; yellow-variegated(f. luteo-variegata) - with yellow-variegated leaves; white-and-white(f. albo-variegata) - with white-variegated leaves; Memminger(f. Memmingeri) - small white spots on the leaves; split-leaved(f. laciniata) - with narrow, deeply unevenly cut leaves; umbrella-shaped(f. umbraculifera) - with a compact, rounded crown; pyramidal (f. pyramidalis) - with a narrow pyramidal crown; undersized(f. pumila) - dwarf; cut-out(f. incisa) - with short and wide, deeply cut leaves; crying(f. pendula).

"Baumannii"The shape of the tree is convex or broadly ovoid, 15-20 m tall, 8-12 m wide, compact in appearance, not as large as the original species. Flowers - large spikes, white, with a red pattern, blooms (from the 10th year) from early to mid-May, the fruits are almost completely absent. The leaves are beautiful, large, up to 25 cm, oblong-elliptic or lanceolate, pitted-palmated, often with crescent-shaped teeth; in autumn the root system is superficial and branched, sensitive to. soil compaction and intervention raises; road surfaces. Prefers warm locations, is frost-resistant, and sensitive to dry air. Soils are moist to moist, slightly acidic to alkaline; slightly heavy soils; doesn't grow on sandy soils; sensitive to salinity. Frost resistance: zone 4.

Horse chestnut family, Horse chestnut genus. The common horse chestnut is a tree, it is also called graceful, this is due to the fact that the trunk is of the correct shape. Also widely used for medicinal purposes. First of all, it is a deciduous tree of the horse-chestnut family. It grows up to 30-35 meters or more, depending on growing conditions.

Common horse chestnut - description, photo and video

It has a large and spreading crown that sways majestically at the slightest breath of wind. Newly blossomed shoots are either grayish-brown or reddish-brown. The leaves have different shape, but basically it is a finger-complex form. The flowers are almost always pale pink or white, collected in cone-shaped inflorescences.

The fruit is a small capsule, inside it is filled with seeds, and outside it is covered with thorns. This tree was named so primarily because, after the leaves fall, a scar remains on the bark, which is very similar to a horse’s horseshoe. This tree blooms in May or June, and the fruits ripen in late August, early September.

Common horse chestnut - in natural conditions, found in the North of India, Southern Europe, East Asia and North America. By the way, it is rightfully considered the homeland North America, this is where most species of this beautiful tree are found.

It prefers to grow in the temperate zone, where the climate is most suitable for this tree, and also loves fertile and fresh soil. Also grows in mountainous areas, Balkan Peninsula, there it is distributed in large quantities. It is in European culture that it has been used for a very long time, or rather since the 16th century.

This type is quite widely used for medical purposes. Not so long ago, scientists specifically studied various alcohol tinctures, decoctions and the like, specifically from this tree and its components. And they came to the conclusion that the alcohol extract of the fruit is most effective for medical purposes. This extract contains many substances such as escin, esculin, and glycosides.

Extracts from this species increase the tone of venous vessels and also accelerate blood flow in the veins. This prevents the formation of such a phenomenon as thrombosis. In addition, preparations made from the components of this tree have anti-inflammatory properties. Also, tinctures from flowers, bark or leaves have been used for quite a long time in folk medicine.

Such tinctures help with rheumatism, vein diseases, and various stomach diseases. But it is worth noting that there is no great need for preparing such tinctures. Since you can go to the pharmacy and buy any drug from the components of this tree.

The common horse chestnut is of quite great economic importance, for example, it has many garden forms, which differ in the shape of leaves, crowns, etc. In Russia, it has been used for quite some time as a landscaping plant; it is planted in parks, gardens, and squares.

But in Russia, it can only grow in southern cities, as it loves a warm climate. As for wood, this type is soft and easy to paint. various colors, and is also used in turning and carpentry. The fruit is used as feed for animals such as sheep and pigs. There is one interesting fact, found out by Stockholm scientists, the whole point is that one such tree can clean about 20 thousand cubic meters of air from harmful exhaust gases.

That is why it is used on such a scale, in gardening construction. This species is also an excellent honey plant; during flowering, it produces a large number of pollen and nectar. The nectar of this tree contains 60-70% sugar. Honey is also unique, it is transparent and viscous, usually has no color at all.

Watch the video Horse chestnut

How beautiful the chestnut blossoms! Its flowers shine like candles, and the air around you seems to glow.

Real or seed chestnut grows on the slopes of the Main Caucasus Range. But you can admire the false or horse chestnut even in middle lane. This tree, reaching a height of 30 meters, is famous not only for its beauty. It gives people health.

Horse chestnut leaves have long been used in medicine in the United States as a source of vitamin K. Preparations made from them are also used in our country as a tonic. The bark and fruits help with chronic disorders of the gastrointestinal tract, hemorrhoids. Atherosclerosis and thrombophlebitis are treated with extract from the bark. Pollen is used to treat prostatitis, varicose veins, as a means of regulating arterial pressure, which improves blood composition. In Azerbaijan, an infusion of chestnut fruits watermelon juice drink for malaria.

Chestnut fruits were used to prepare especially valuable and medicinal types of beer, such as royal beer. For three liters of water, take 10-20 (depending on size) peeled horse chestnut fruits. They must be cut into halves, but not smaller, otherwise the drink will be bitter. Place the chopped chestnuts in a bag with a sinker, put them in a jar, add 1 cup of sugar and 1 teaspoon of sour cream. Cover with three layers of gauze and place in a dark, warm place. Fermentation will continue for two weeks, after which you will get a very pleasant foaming drink. It not only quickly removes radionuclides from the body, but supplies calcium, copper, cobalt and iodine. You should drink this beer for a month, 3 times a day, half a glass or as much as you want, 15-20 minutes before meals. The amount of water and sugar corresponding to the decrease is added daily.

The drink is also useful for children over one year old. It heals the body and allows you to get rid of many diseases. Practice shows that this is a real elixir of youth, partially restores hair color and improves general state. Just don’t forget with sweet water periodically add chestnuts - then the beer will last for several months. (Zoya Kovalenko, Moscow).

Common horse chestnut(lat. Aesculus hippocastanum) is a large deciduous tree, the most famous species of the Horse chestnut genus in Russia. Grows on small area in the mountains of the Balkans (in the north of Greece, Albania, the Republic of Macedonia, Serbia and Bulgaria) in deciduous forests along with alder, ash, maple, hornbeam, linden, beech and other tree species, rising into the mountains to a height of 1000-1200 m above level seas. It is found in the mountainous regions of Iran and in the foothills of the Himalayas. Widely cultivated in the temperate climate zone, common in plantings in many regions of the European part of Russia.

Long-lasting (under favorable conditions reaches an age of 200-300 years). Almost not damaged by insects. Tolerates transplantation well in adulthood.

Shade-tolerant, grows well in deep, loose soils - clay or sandy loam, sufficiently moist, but without excessive moisture. Tolerates fairly dry chernozem soils in the steppe zone, it does not tolerate saline soils well. Sensitive to dry winds, which is why the leaves often burn badly in summer and fall off prematurely.

Winter-hardy in cultivation in the central zone of the European part of Russia (up to Moscow). At the latitude of Moscow, in very severe winters it freezes; Young trees also freeze in St. Petersburg, but in protected places they grow into large, abundantly flowering trees.

Materials used:

• Z. Kovalenko.

Horse chestnut, common- an indigenous plant in Western Asia, currently widely cultivated in parks, gardens and along city streets in many countries around the world, in Ukraine (Kyiv), as well as in Europe and the United States of America. Horse chestnut flowers have a delicate honey scent. The common horse chestnut is often called simply "horse chestnut", but it must be distinguished from other members of the horse chestnut genus.

Horse chestnut prefers to grow in deep, loamy, well-drained soils. A very decorative and fast-growing tree, which is considered very hardy. However, it tends to suddenly drop old heavy branches, so it requires pruning. The horse chestnut (common) tree begins to bear fruit 20 years after the seeds are planted.

The seeds germinate very quickly and require protection from harsh weather conditions. The seed has a very limited viability time and should not dry out. Stored horse chestnut (common) seeds should be soaked for 24 hours before sowing. It is best to sow the seeds with the white spot facing down.

ATTENTION! Horse chestnut seeds contain toxic saponins, which give them a bitter taste. They are poisonous to humans, so eating raw chestnuts is strictly contraindicated.

Saponins are also toxic to fish, and Native American hunting tribes traditionally placed large quantities of chestnut seeds in streams, lakes and other bodies of water to stun or kill fish. Some mammals, such as deer, can eat chestnut fruit without harm. There are known cases of using the fruits of horse chestnut (ordinary) as feed for livestock.

Contraindications

Individual intolerance, allergies. Be careful with dosages. Pregnancy and lactation - only after consultation with a doctor. It is not recommended to eat horse chestnut seeds, even after processing, for people with kidney or liver diseases.

Horse chestnut preparations are contraindicated in case of allergy to plants of the horse chestnut family Hippocastanoideae.

Despite the fact that they exist popular recommendations on the use of horse chestnut (ordinary) for mastitis (infants) - preparations of horse chestnut (ordinary) should not be used during pregnancy and lactation without medical prescription and supervision.

Adverse reactions: in some cases, gastrointestinal disorders such as nausea and stomach discomfort are observed. Allergic reactions are also possible.

The use of horse chestnut (ordinary) in cooking

Roasted seeds are used as a coffee substitute. However, toxic saponins from the seeds must be removed before consumption - this process also removes many minerals and vitamins, leaving mainly starch. Once the toxins are leached, the seeds can be dried, ground into powder and consumed as a porridge.

Horse chestnut (common) chestnut seeds contain up to 40% water, 8-11% protein and 8-26% toxic saponins, which must be leached for the seeds to be safe to eat.

American Indians did it in the following way: the nuts were slowly burned (to render the saponins harmless), and then, after cutting them into thin slices, they were placed in a cloth bag and washed in running water within 2-5 days. However, even after this, it is not recommended to eat large quantities of chestnut seeds.

The use of horse chestnut (ordinary) in medicine

Horse chestnut is used as an astringent and anti-inflammatory agent. Also as a remedy that helps improve the tone of venous walls that sag or stretch, which can cause bleeding or other diseases. It also reduces fluid retention by increasing capillary permeability. Constricts blood vessels, thereby increasing blood pressure. Promotes healing.

Horse chestnut (common) bark is used as an anti-inflammatory, astringent, diuretic, antipyretic, tonic and vasoconstrictor.

Used in small doses internally to treat a wide range of vascular diseases, including arteries, varicose veins, phlebitis, leg ulcers, hemorrhoids and. It is also included in lotions and gels for external use.

Horse chestnut bark tea is used in the treatment of dysentery and externally in the treatment of lupus and skin ulcers. Tea made from the leaves is used as a tonic to treat fever and whooping cough.

Oil obtained from horse chestnut seeds was used externally as a treatment for rheumatism.

Parts used: bark that is collected in the fall is preferable to the bark of young branches. Sometimes collected in the spring and dried for later use. Chestnut seed - Semen Hippocastani.

Organoleptic properties of seeds: the smell is light, the taste is bitter, acrid.

Preparations:"Eskuzan" for , "Esflazid" for varicose veins, and others.

Uses of horse chestnut (common) that are supported by clinical evidence: internally, to treat symptoms of chronic venous insufficiency, including pain, heaviness in the legs, nighttime, etc. Externally, for the symptomatic treatment of chronic venous insufficiency, sprains, etc.

Uses described in pharmacopoeias and systems traditional medicine: treatment .

The use of horse chestnut (ordinary) in folk medicine

Horse chestnut (common) is used in alternative medicine as an analgesic, hemostatic and wound healing agent.

Uses of horse chestnut (common) described in folk medicine, not supported by experimental or clinical data: treatment of bacillary dysentery and fever. Also, as a hemostatic agent for excessive menstrual flow or other gynecological bleeding, and as a tonic.

Economic use of horse chestnut (common)

The seed contains variable amounts of saponins. Starch obtained from seeds can be used for washing (to stiffen fabrics).

A yellow dye is obtained from horse chestnut bark. The flowers contain the yellow antioxidant dye quercetin.

Horse chestnut wood (ordinary) is soft, light and not durable. It has little commercial value and is mainly used in making furniture, jewelry boxes and charcoal.

Synonyms: Aesculus asplenifolia, Aesculus castanea, Aesculus memmingeri, Aesculus procera.

Botanical description

A tall (up to 30 m) deciduous tree with a wide dense crown of the horse-chestnut family (Hippocastanaceae). The leaves are opposite, long-petiolate, palmately compound with 5–7 sessile, obovate, elongated, pointed leaves. The flowers are irregular, white with red-pink spots, collected in erect pyramidal panicles. Blooms in May. The fruit is a round capsule up to 6 cm in diameter, covered with large soft spines, inside which there are 1–2 large brown shiny seeds. The fruits ripen in September–October.

Geographical distribution

IN wildlife found as a relict plant in the mountain forests of the Balkan Peninsula (Albania, Greece, Yugoslavia). It has been cultivated in Europe and Ukraine since the 16th century. in gardens and parks as an ornamental plant.

Medicinal raw materials

WITH therapeutic purpose and the bark of young branches is used to make medicines (Cortex Aesculi hippocastani), sheet (Folium Aesculi hippocastani), flowers (Flores Aesculi hippocastani) and fruits (Fructus Aesculi hippocastani). The bark is collected in the spring, cut into pieces and dried immediately after collection in the open air or in a well-ventilated area. The flowers are harvested in May, dried the first day in the sun, and then under a canopy or indoors. The leaves are harvested from May to September, until they turn yellow, with or without petioles. Dry in the fresh air under a canopy or in a well-ventilated area, spreading it in a thin layer (2–3 cm). Fully ripe fruits are harvested when they begin to fall. Dry them under a canopy or in a well-ventilated area at temperatures up to 25°C.

The official raw materials in Ukraine are chestnut leaves and fruits.

In other European countries to receive medicines The bark of branches, peel of fruits and flowers of the plant are also used.

Biologically active substances

The pharmacological activity of horse chestnut fruits is associated with the content of the coumarin glycoside esculin (esculoside) and its aglycone esculetin (escinol), the oxycoumarin glycoside fraxin and its aglycone fraxetin, as well as the triterpene saponin glycoside β-amyrin type escin (content up to 13%).

Further chemical analysis showed that escin is a mixture of several substances: α-escin, β-escin and cryptoescin (H. Wagner et al., 1970), or escins Ia, Ib, IIa, IIb and IIIa (N. Murakami et al., 1994), aglycones of which are escigenin, protoescigenin, baringtogenins C and D.

Aescins IIIb, IV, V and VI, isoescins Ia, Ib and V were also found in horse chestnut fruits (M. Yoshikawa et al., 1998). The main component determining the biological activity of escin is β-escin. When studying the drug escin (manufactured by JSC Galychfarm) using liquid chromatography, it was found that the content of β-escin in it is 76.35–79.29% (A.V. Shovkovy and A.T. Shein, 1999). Along with escin, chestnut fruits contain other saponin glycosides. In particular, the acid hydrolysis of the saponin fraction yielded sapogenols hypocaesculin (21-O-angeloyl-22-O-tigloyl-R1-baringenol or 21-O-tigloyl-22-O-angeloyl-R1-baringenol) and baryngtogenol-C-21 -angelat (T. Konoshima and K. H. Lee, 1986).

Aescins Ia, Ib, IIa and IIb were also identified in Japanese chestnut fruits A. turbinata Blume (M. Yoshikawa et al., 1999).

In addition to the already known ones, new triterpene saponins were found in the fruits of the Chinese chestnut Aesculus chinensis (X. W. Yang et al., 1999; J. Zhao et al., 2001):

In addition, the fruits of the common chestnut contain about 0.13% flavonoid glycosides (quercitrin, isoquercitrin, quercetin and kaempferol), about 0.9% tannins (catechin tannins), fatty oil (5–7%), proteins (11% ), pectins, starch (up to 49.5%).

Chestnut flowers and leaves are also rich in flavonoids - derivatives of kaempferol and quercetin. Specifically, the leaves contain kaempferol 3-glucoside, kaempferol 3-arabinoside, kaempferol 3-rhamnoglucoside, quercitrin, isoquercitrin, rutin and sireoside. In addition to flavone glycosides, chestnut flowers contain mucus, tannins and pectin substances, and leaves contain pectin substances and carotenoids (lutein, violaxanthin).

Chestnut bark contains the coumarin glycoside esculin (3%) and its aglycone esculetin, escin, the oxycoumarin glycosides fraxin and scopolin and their aglycones (fraxetin and scopoletin), the flavonoid quercetin, tannins (in particular, the catechol dimer proanthocyanidin-A2), phytosterols ( stigmasterol, α-spinasterol, β-sitosterol), fatty oil (2.5-7%), sugars (9%), ascorbic acid, thiamine, phylloquinone.

History of use in medicine

The first mention of the use of chestnut for medicinal purposes appeared in 1556. Physician Peter Andreas Mattioli (1500–1577) recommended giving horse chestnut fruit to horses that suffered from shortness of breath. In 1575, the botanist Clausius brought chestnut seedlings from Turkey and planted them in Vienna as ornamental trees. In 1615, chestnuts were planted in France, and 200 years later they appeared in America. Since 1842, Kyiv began to be landscaped with chestnuts. Some botanists of that time believed that the chestnut came from India, as indicated by its French name - "Marronier d'Inde". Only in the 19th century. It was found that the birthplace of chestnut is the mountain forests of the Balkan Peninsula.

The American Indians prepared a puree from the poisonous horse chestnut fruits roasted on hot stones, then soaked it in lime water for several days and used it to make flour. From the germinated seed, which becomes palatable due to the transformation of bitter substances into sweet ones, they prepared malt. C. L. Millspaugh (1974) believes that the Indians used the seed skin as narcotic substance(in terms of activity, 10 g was equivalent to 3 g of opium). Powder from the seeds and crushed branches was used to poison fish.

In folk medicine of the countries of southern Europe in the 18th-19th centuries. Chestnut fruits and bark were used as a substitute for cinchona bark to treat malaria, febrile conditions and amoebic dysentery. These remedies were especially popular in France, which was due to the political isolation of the country during the reign of Napoleon II and the cessation of imports of expensive cinchona bark. However, as historical sources indicate, chestnut remedies were weaker in action than cinchona bark. Later there were reports that chestnut treats some diseases associated with impaired blood circulation. Powder from the fruit was sprinkled on varicose ulcers. In 1708, Tabler reported the effectiveness of the decoction in the treatment of hemorrhoids. Since 1866, chestnut tincture began to appear in European pharmacies, which was prescribed for chronic intestinal inflammation, gout and hemorrhoids.

Horse chestnut was introduced into scientific and practical medicine by the French physician A. Artault de Vevey. In 1896 in a French magazine “Revue de théérap. meed. chirur." his publications appeared about successful treatment hemorrhoids and varicose veins with chestnut tincture. The famous French herbalist Leclerc considered chestnut effective means for the treatment of prostatitis and prostate adenoma. In the 50s of the twentieth century. production of chestnut venotonic preparations began in Germany.

Herbal preparations of horse chestnut are still widely used in folk medicine in many countries today. Chestnut flower tincture has anti-inflammatory and analgesic properties, the seed has anti-inflammatory properties, and the seed peel has hemostatic, anti-inflammatory and analgesic properties. Fresh flower juice is prescribed orally for varicose veins, thrombophlebitis, atherosclerosis and hemorrhoids. Flower juice preserved with alcohol, tincture of flowers or fruits are recommended orally and topically for varicose veins and hemorrhoids, and as a rub for arthritis, rheumatic and gouty pain. A decoction of fruit peel is prescribed locally (baths, douching) for uterine and hemorrhoidal bleeding. Chestnut seed powder is used for colds and respiratory diseases.

Decoctions and infusions of chestnut bark have astringent, hemostatic, anti-inflammatory, analgesic and anticonvulsant properties. They are used as effective internal and external remedies for prolonged diarrhea, chronic colitis, increased acidity of gastric juice, respiratory tract diseases (chronic bronchitis), and malaria. They are recommended as a hemostatic agent for hemorrhoidal and internal bleeding, especially uterine bleeding.

Infusion of bark, tincture of fruits, infusion of fruit peel and fresh rubbed chestnut leaves are also used as an external remedy for dressing suppurating wounds.

Pharmacological properties

A study of the pharmacological activity of chestnut herbal preparations (alcoholic extract, alcoholic tinctures, decoctions and infusions of leaves, flowers and fruits) showed that the most effective is the alcoholic extract of the fruit, which has low acute toxicity.

Chestnut fruit extract stimulates cardiac activity in cold-blooded animals, reduces blood pressure in cats by 15–70%, in small doses dilates the vessels of the isolated ear of a rabbit, and in higher doses narrows them. In experimental thrombophlebitis in dogs, chestnut extract reduces the general inflammatory response and local swelling. In people without pathology of peripheral blood vessels, it was found that the fruit extract increases the tone of the veins of the lower leg.

In addition, it exhibits anti-inflammatory, decongestant, analgesic and capillary-strengthening properties, reduces blood viscosity, and prevents the development of stasis in capillaries.

The purified total extract of horse chestnut fruit promotes the reverse development of experimental cholesterol atherosclerosis in rabbits, normalizes the content of cholesterol and lecithin in the blood, and reduces lipoidosis of the aorta and liver.

The pharmacological activity of horse chestnut herbal preparations is associated mainly with the content of the triterpene saponin glycoside escin and its derivatives. Like other saponins, escin has hemolytic activity, but it does not manifest itself in therapeutic doses. In contrast to crystalline β-escinic acid, which is almost insoluble in water, the water-soluble aescinic forms of α-escinic acid, sodium α-escinate and amorphous β-escinic acid are well absorbed from the gastrointestinal tract. Sodium β-escinate and amorphous β-escinic acid when administered orally and escin when administered subcutaneously have pronounced anti-inflammatory and anti-edematous properties, improve tissue trophism with insufficient blood supply and edema.

The anti-inflammatory properties of escin and its derivatives have been confirmed in numerous experiments on different models inflammation. They inhibit the development of experimental edema of the paw of rats caused by ovalbumin, histamine, serotonin, burns or stagnation (lymphatic edema), application of locally irritating substances (chloroform). Escin dose-dependently reduces (by a maximum of 70%) the permeability of the plasma-lymphatic barrier caused by the injection of bradykinin into the paw of rabbits (M. Rothkopf and G. Vogel, 1976), prevents the occurrence of an exudative reaction to the administration of prostaglandins E1 and F2a (M. Rothkopf-Ischebeck and G. Vogel, 1980; D. Longiave and al., 1978). A similar effect of escin appears in models of ultraviolet erythema (R. Eisenburger et al., 1976), inflammation of the mucous membrane Bladder rats induced by electrocoagulation (P. Strohmenger and H. Wenzel, 1976), post-ischemic muscle edema and cerebral edema caused by cold injury (M. Arnold and M. Przerwa, 1976). Escin dose-dependently inhibits the development of formalin peritonitis and carrageenan pleurisy in rats (Rothkopf and G. Vogel, 1976; M. Guillaume and F. Padioleau, 1994); reduces the amount of exudate, its protein content, and the migration of leukocytes into the pleural cavity. It has been established that with an increase in the dose of escin, the exudation of small molecules into the abdominal cavity is more effectively inhibited compared to large molecules.

The ability of purified preparations of escins Ia, Ib, IIa and IIb at a dose of 50–200 mg/kg to suppress the initial exudative stage of inflammation was confirmed by H. Matsuda et al. (1997) on different experimental models: inflammation of the skin of rats and mice in response to the introduction of acetic acid, ovalbumin, dextran, trypsin, hyaluronidase, kaolin, bee venom, carrageenine, histamine, bradykinin and the Arthus reaction. Escins, with the exception of escin Ia, prevent the increase in vascular permeability under the influence of serotonin. No effect was observed in models of the late (proliferative) phase of inflammation. However, other researchers point to the ability of escin and its hydrolysis products to inhibit the development of cotton wool granuloma in rats (R. Eisenburger et al., 1976), a reaction to implantation of plastic foam (M. Guillaume and F. Padioleau, 1994; M. Przerwa and M. Arnold, 1975).

Of great importance in the development of the antiexudative effect of escin is its ability to increase vascular resistance, which has been proven in various models of inflammation in the Evans blue test (Rothkopf and G. Vogel, 1976), as well as by the results of a petechial test in guinea pigs that were on a scorbutogenic diet Escins, especially its sapogenin escinol, inhibit hyaluronidase activity (IC50 149.9 µM and 1.65 µM, respectively) (R. M. Facino et al., 1995). Thus, the basis of the anti-inflammatory effect of escin is the strengthening of capillary walls. Escin reduces the number of pores in the walls of capillaries and their diameter. In experiments on animals, it was found that escin has an anti-exudative effect that is 600 times greater than the classic flavone rutin. As shown in models of formaldehyde peritonitis, experimental pleurisy in rats and swelling of the rabbit's paw, the anti-exudative potential of escin is comparable to the effect of acetylsalicylic acid, hydrocortisone, phenylbutazone and butadione, and in some cases even exceeds them. There is an assumption that the anti-inflammatory effect of escin is associated with its effect on the adrenal cortex and the ability to stimulate the secretion of glucocorticoids.

Escin has pronounced membranotropic properties. By binding to the lipids of biological membranes, it increases the fluidity of the lipid bilayer (L.V. Ivanov et al., 1988). Considering that escin binds much more strongly to the membranes of erythrocytes and vascular wall cells than to liposomes (which consist of phospholipids), one can also assume its ability to react with membrane proteins. Such an interaction is possible between the glucuronic acid residue and the amino acid residues of lysine and arginine. Experiments studying the fluidity of lipids in the vascular wall indicate that the increase in vascular resistance in the presence of escin occurs due to an increase in their elasticity and is not associated with compaction of vascular tissue. The increase in lipid fluidity partially explains the vasotonizing effect of the drug. The membrane-stabilizing effect of escinol, escin and esculoside was demonstrated in experiments studying the resistance of erythrocytes to osmotic hemolysis. The optimal active concentration of escin of 10-5 G corresponded to the level of the drug in the blood of patients after taking a therapeutic dose (L. A. Chaika and I. I. Khadzhai, 1977). Escin, as a saponin, reduces the surface tension of the liquid, is well adsorbed at the interface of surfaces, and these effects extend to the vascular wall. Escin increases the wettability of capillaries, which facilitates the flow of tissue fluid directed into the capillary. Thus, the fluid that predetermines perivascular edema is directed into the vessels due to increased oncotic pressure inside the capillaries.

Important mechanisms of the anti-inflammatory and anti-edematous action of escin are also its venotonic effect. The pronounced venotonic properties of escin were confirmed in experimental studies in vitro on the portal and saphenous vein of rabbits, the saphenous vein of dogs, as well as on segments of normal and varicose v. saphena human (EC50 9.4–15.9 µM/l). In a study of normal and slightly dilated veins with valve insufficiency, the effect obtained was 70–71% of the maximum possible contraction under the influence of KCl and 43% of the contraction due to norepinephrine. However, veins deeply affected by varicose veins responded to escin weaker - the venotonic effect was only 10% of the maximum possible (F. Brunner et al., 2001). These results confirm the greater therapeutic effectiveness of escin in the early stages of varicose veins. The venotonic effect of escin in the study of segments of normal human saphenous vein persisted for an hour after removal of the drug from the incubation medium.

By maximum effect escin was superior to acetylcholine and vasopressin and was equal to the activity of serotonin and dihydroergotamine. However, the affinity of the venous wall for escin is lower compared to the listed venotonics, which indicates non-reversible venodilation under the influence of escin (F. Annoni et al., 1979). On the perfused saphenous vein of dogs, the venotonic effect of escin lasts more than 5 hours; the drug predetermined an increase in venous pressure, and also significantly enhanced the contractile effect of norepinephrine. In vivo studies in dogs demonstrate improvements in femoral vein elasticity (M. Guillaume and F. Padioleau, 1994). It is assumed that the venotonic effect of escin is due to stimulation of the synthesis and release of prostaglandin F2a in the venous wall. But when isolated rat lungs are perfused with a solution containing escin, the release of this prostaglandin increases (F. Berti et al., 1977). The pronounced effect of escin on the process of tight closure of venous valves is important in improving venous circulation and preventing reflux. The use of escin allows you to achieve an effect that is 90% of the maximum possible as a result of the action of norepinephrine.

Increasing the tone of the veins facilitates the reverse flow of blood from tissues to the heart, improves the flow of lymph through the thoracic lymphatic duct by 70%. In addition, with intravenous administration of escin, the content of adrenaline in the adrenal glands decreases and blood pressure increases, and with perfusion of isolated adrenal glands, a vasoconstrictor effect is observed. Obviously, the combination of these effects also contributes to the manifestation of the anti-edematous effect of escin.

The venotonic and anti-inflammatory activity of escin provides its therapeutic effect for varicose veins. In the occurrence of varicose veins, not only venous stasis plays an important role, but also the activation of endothelial cells under hypoxic conditions. On the model ex vivo An isolated human umbilical vein perfused under hypoxia showed that escin inhibits two important events that are prerequisites for the activation of endothelial cells during hypoxia. It counteracts the decrease in ATP content in endothelial cells and the subsequent activation of phospholipase A2, an enzyme that ensures the release of the precursor of platelet activating factor (PAF) from cell membranes and arachidonic acid- a precursor to inflammatory modulators - leukotrienes and prostaglandins. Using scanning electron microscopy, inhibition of adhesion of neutrophils and neutrophil-like cells of the HL60 line to the venous wall in the presence of escin was demonstrated. Inhibition of hypoxic activation of endothelial cells of the venous wall manifested itself at an escin concentration of 100 ng/ml and reached a maximum at a concentration of 750 ng/ml (T. Arnould et al., 1996). At the same time, the production of superoxide anions and leukotriene B4 in the system decreased (C. Bougelet et al., 1998). The antiradical properties of escin have been confirmed by other researchers - it dose-dependently inhibited enzymatic and non-enzymatic lipid peroxidation in vitro(EC 5–500 µg/ml) (M. Guillaume and F. Padioleau, 1994). Thus, the presented results of experimental studies indicate that escin inhibits hypoxia-induced activation of endothelial cells, which determines increased adhesion of neutrophils, and their mediators and proteases contribute to the destruction of the intercellular matrix and cause damage to the venous wall, which is microscopically reminiscent of the changes observed in varicose veins. By reducing the manifestations of inflammation and damage to the venous wall, escin inhibits the release by activated cells of growth factors involved in the proliferative phase of inflammation, which contribute to the maintenance of venous insufficiency and the development of varicose veins (R. W. Frick, 2000). Escin maintains the endothelium in an intact state under conditions of venous stasis, prevents the recruitment, adhesion and activation of neutrophils, acts as an antagonist of inflammatory mediators, thereby preventing damage to the venous wall. These data, along with the results of studying venotonic activity, once again emphasize the special value of the preventive use of escin preparations in the early stages of varicose veins.

It is important that other biologically active substances contained in total chestnut extracts potentiate the anti-inflammatory effect of escin. Thus, in the presence of the natural flavonoid complex of chestnut (1:10), the activity of escin increases 5 times. Petroleum extract of chestnut bark also has anti-inflammatory properties. (F. Senatore et al., 1989).

The antiexudative and capillary-strengthening properties of escin make it possible to use it for cerebral edema, which was first proven experimentally in 1967 by S. Gorini and R. Caponi in animals with cerebral edema due to craniotomy. Further experimental studies confirmed the effectiveness of the drug in traumatic brain edema. (T. Tzonos and H. Riebeling, 1968; L. Auer, 1975) and ischemic (M. Cerisoli et al., 1981) genesis Traumatic brain injuries are characterized by vasogenic cerebral edema, which is based on increased vascular permeability.

In the future, it is aggravated by cytotoxic edema - swelling of brain tissue, which is based on metabolic disorders caused by the traumatic factor itself, vasogenic cerebral edema and the toxic effect of tissue breakdown products. Slow resorption of blood from brain tissue and the cranial cavity promotes the accumulation of under-oxidized and toxic tissue breakdown products, increasing osmolarity and hydration (edema and swelling) both locally at the site of injury and throughout the brain. These processes lead to an increase in the lesion, the development or increase in intracranial hypertension, compression and displacement of the brain. Cerebral edema and intracranial hypertension are always accompanied by a decrease in venous tone, impaired venous outflow, stagnation of venous blood in the cranial cavity with the development of venous hypertension, which contributes to the development of destructive edema. By restoring damaged vascular permeability and increasing venous tone, escin prevents the development or eliminates disturbances of venous outflow, venous hypertension and cerebral edema. Reducing the phenomena of cerebral edema and improving venous outflow, in addition, contributes to the normalization of cerebral circulation, which in turn creates favorable conditions for speedy resolution (resorption) of the focus of brain contusion and hematoma. By eliminating disturbances in the permeability of the vascular wall and increasing the tone of the veins, as well as eliminating edema of various brain structures, escin significantly prevents the development of pathophysiological mechanisms underlying pain stimuli, and thus exhibits an analgesic effect.

Escins Ia, Ib, IIa and IIb enhance the evacuation function of the stomach of mice (H. Matsuda et al., 2000), inhibit (especially escins IIa and IIb) the absorption of alcohol in the gastrointestinal tract of rats (N. Murakami and I. Kitagawa, 1994).

When administered orally to mice (10–50 mg/kg), escins Ia, Ib, IIa and IIb markedly inhibit the development of ethanol gastric damage (H. Matsuda et al., 1999). The gastroprotective effect of escins is suppressed when animals are given capsaicin (which blocks afferent autonomic nerve fibers), N(G)-nitro-L-arginine methyl ester (NO synthase inhibitor) and indomethacin (an inhibitor of prostaglandin synthesis), as well as in animals with streptozocin diabetes (with abnormal sympathetic activity nervous system). Deacylated escin derivatives are not active in this regard. In the perfused stomach of anesthetized rats, the ability of escin (at doses of 10 and 50 mg/kg) to inhibit the secretion of hydrochloric acid stimulated by histamine and carbachol was demonstrated. (E. Marhuenda et al., 1994). E. Marhuenda et al. (1994) note that indomethacin neutralizes the effect of escin on ethanol damage to the gastric mucosa, but they did not find an increase in the production of prostaglandin E2. Thus, the mechanisms of the gastroprotective action of escin have not been fully elucidated. Apparently, it is due in part to the antisecretory activity of the drug, and in part is mediated by endogenous prostaglandins, nitric oxide, capsaicin-sensitive afferent neurons and the sympathetic nervous system.

Escins Ia, Ib, IIa and IIb exhibit hypoglycemic effects in animal experiments with oral glucose loading (N. Murakami and I. Kitagawa, 1994; M. Yoshikawa et al., 1996). In normal animals, as well as when glucose is administered intraperitoneally, the hypoglycemic effect of escins is not observed. It has been established that escins Ia and IIa do not have insulin-like activity and cannot stimulate insulin production. Their hypoglycemic effect is associated with inhibition of glucose absorption in the small intestine (H. Matsuda et al., 1998).

Esculoside (esculin), due to the inhibition of hyaluronidase activity, stabilizes capillaries, stimulates the antithrombotic activity of blood serum, and blocks the inhibition of antithrombin synthesis by cells of the reticuloendothelial system. Escin also improves the rheological properties of blood. Thanks to this, horse chestnut preparations promote venous outflow, improve microcirculation, counteract the occurrence of stasis in capillaries, and have a beneficial effect on tissue trophism. Normalizing the balance between intravascular pressure and the strength of the vessel wall prevents the occurrence of hemorrhages.

The anticoagulant effect of horse chestnut preparations is also associated with Fraxin. But in general, in terms of anticoagulant properties, they are inferior to dicoumarin.

In experiments in vitro escin at a concentration of more than 10 μg/ml significantly reduces the period of crystallization of uric acid. In experiments on rats, esculoside exhibits moderate saluretic activity, dose-dependently increasing the level of renal excretion of chlorides, sodium and potassium. The diuretic activity of escin is much weaker; at the highest dose studied, the minimal effect of esculoside is achieved (M. J. Martin et al., 1990).

The experiment demonstrated a weak antispasmodic (papaverine-like) effect of esculetin, esculin, fraxin and fraxetin on the smooth muscles of internal organs and coronary vessels.

Experiments on rats indicate that the catechol dimer proanthocyanidin-A2 of chestnut bark improves trophism skeletal muscles normally and after their traumatic denervation (P. Ambrogini et al., 1995).

There is evidence that saponins (in particular, esculetin) and compounds of the peptide nature of chestnut fruits inhibit the growth of some bacteria and fungi. Aescins IVc, IVd, IVe and IVf from the seed of Aesculus chinensis have properties as inhibitors of the BOL-1 protease (X. W. Yang et al., 1999).

Chestnut extract, when administered intraperitoneally, inhibits the growth of Ehrlich ascitic carcinoma and lymphosarcoma 150 implanted in mice, and when studied on a chicken embryo, lymphosarcoma and C3H carcinoma. It has been established that it does not have antimitotic activity, but after a short incubation with tumor cells (for 30 seconds) it causes irreversible morphological changes in them. It has been established that the antitumor properties of chestnut extract against KB line cells are associated with the saponin fraction, in particular with the sapogenols hypocaesculin and barynthogenol-C-21-angelate obtained from its acid hydrolysis (T. Konoshima and K. H. Lee, 1986).

At local application(cutaneously) aescin and labeled sodium 3H-escinate have been proven in experiments on mice, rats and pigs that it quickly penetrates into nearby areas of the skin and muscles. Resorption of escin into internal organs, blood, urine, skin and muscles of other areas is limited. The concentration of labeled escin in the dermis is 50–600 times, and in muscles 10–50 times higher than in the blood. Only 0.5–1% of escin is excreted in urine over 24 hours. It is estimated that the total elimination of the drug in urine and bile is 1–2.5% of the administered dose (W. Lang, 1977). When administered intravenously, escin is quickly eliminated from the body with urine and bile, and when oral administration relatively quickly absorbed mainly from the duodenum.

Methods for radioimmune and enzyme immunoassay of escin concentration in blood serum have been developed in order to study the bioavailability and pharmacokinetics of its preparations (T. Lehtola and A. Huhtikangas, 1990; C. Hentschel et al., 1994).