JP2012530700A - Cosmetic composition containing chestnut skin extract - Google Patents

Abstract

  The present invention relates to a cosmetic composition for alleviating or suppressing pruritus comprising a chestnut skin extract as an active ingredient. The chestnut skin extract contained in the cosmetic composition according to the present invention, in one embodiment according to the present invention, suppresses the activity of proteolytic enzyme activity receptor-2 (PAR-2), which is a source of irritation for itching As a result, it was confirmed that an excellent itch reduction or suppression effect can be exerted, and thus it can be used as an active ingredient of a cosmetic composition for the reduction or suppression of itch.

Description

  The present invention relates to a cosmetic composition containing chestnut skin extract.

  Itching is defined as an unpleasant skin sensation that triggers the desire to scratch, and the skin is exposed to harmful external stimuli as a physiological self-protection mechanism such as pain, touch, coldness or heat Sometimes it recognizes this and protects the skin.

  Itching is a common symptom that often appears in various skin and systemic diseases, and acute itching due to side effects of urticaria and various drugs can be easily cured, but biliary atresia or kidney disease or atopy The fact is that it is very difficult to treat severe chronic itching such as disease.

  Itching is triggered by a variety of causes, including inflammation, cancer, metabolic diseases, infections, psychiatric illnesses, drug administration or stress, and several recent studies have shown that itching of the skin and peripheral and central nervous systems It reveals that organic connections are deeply involved in the response and regulation of stimuli that induce itching.

  Recently, it has become clear that certain sensory neurons and their receptors react specifically to itching, and itching is no longer a subordinate aspect of pain, but is accepted as an individual sense of the sensory nervous system. It is considered that different itch mediators and their receptors are involved in various itch-inducing diseases (Steinhoff et al., Journal of Investigative Dermatology, 126, pp 1705-1718, 2006).

  Although histamine has been mainly used in experiments for itch studies so far, chronic itch diseases such as atopy are caused by neurological causes rather than by histamine-dependent pathways. There has been an allegation that this explains why antihistamines are not effective in itching of atopic diseases (Stander et al., Experimental Dermatology, 11, pp12-24, 2002). ).

  In addition, the first generation antihistamine is mainly used for systemic administration, but has anti-parasympathetic action and sedation, and chlorpheniramine, the first generation antihistamine, is administered to patients with atopic dermatitis when administered locally. It is known that itching cannot be suppressed (Munday et al., Dermatology, 205, pp40-45, 2002), and the use of topical antihistamines for atopic dermatitis is due to the risk of skin hypersensitivity reactions. Not recommended. Ebastine and terfenadine, which are second-generation antihistamines that have no sedation, may cause arrhythmia when taken with drugs that inhibit cytochrome P450 activity (ketoconazole, erythromycin) (Hey et al., Arzneimintegrford, 46). pp 159-163, 1996), and associated side effects occur.

  Accordingly, there is an urgent need for the development of an effective palliative relief agent that is efficient and has few side effects, particularly an effective palliative agent for chronic itch disease such as atopy.

Steinhoff et al. , Journal of Investigative Dermatology, 126, pp 1705-1718, 2006. Standard et al. , Experimental Dermatology, 11, pp12-24, 2002 Munday et al. , Dermatology, 205, pp40-45, 2002. Hey et al. , Arzneimitterforschung, 46, pp159-163, 1996.

  Accordingly, an object of the present invention is to solve a technical problem that has been conventionally required. Specifically, an object of one embodiment of the present invention is to provide a cosmetic composition for reducing or suppressing pruritus including a chestnut skin extract and a cosmetic composition for immunosuppression.

  For this purpose, one embodiment according to the present invention includes a chestnut skin extract as an active ingredient, which has an excellent effect of suppressing or alleviating pruritus while reducing the side effects of conventional pruritus treatment agents. The present invention relates to a cosmetic composition for reducing or suppressing pruritus.

One Example which concerns on this invention is related with the cosmetic composition for skin barrier function improvement which contains a chestnut skin extract as an active ingredient.
One Example which concerns on this invention is related with the cosmetics composition for immunosuppression which contains a chestnut skin extract as an active ingredient.

  One embodiment according to the present invention relates to a cosmetic composition for improving or treating atopic dermatitis comprising a chestnut skin extract as an active ingredient.

  The cosmetic composition according to the present invention contains a chestnut skin extract as an active ingredient, thereby allowing the activity of proteinase-activated receptor-2 (PAR-2), which is a source of irritation to itch. It is possible to exert an excellent alleviation or suppression of pruritus through suppression of the skin, and to fundamentally treat immune hypersensitivity reactions that can cause pruritus through the immunosuppressive activity of chestnut skin extract .

It is the graph which showed the measurement result of the PAR-2 activity inhibitory effect (trypsin process) of the chestnut skin extract based on one Example of this invention. It is the graph which showed the measurement result of the PAR-2 activity inhibitory effect (SLIGKV process) of the chestnut skin extract based on one Example of this invention. It is the graph which showed the measurement result of the PAR-2 activity inhibitory effect (trypsin, SLIGKV treatment) of the chestnut skin 1,3-butylene glycol (BG) extract based on one Example of this invention. It is the graph which showed the TNF- (alpha) secretion reduction effect of the chestnut skin extract based on one Example of this invention. It is the graph which showed the IL-6 secretion reduction effect of the chestnut skin extract based on one Example of this invention. It is the graph which showed the IL-1 (alpha) secretion reduction effect of the chestnut skin extract based on one Example of this invention. It is the graph which showed the IL-8 secretion reduction effect of the chestnut skin extract based on one Example of this invention. It is the graph which showed the GM-CSF secretion reduction effect of the chestnut skin extract based on one Example of this invention. It is the graph which showed the IL-6 secretion decreasing effect by the trypsin and active peptide (SLIGKV) of a chestnut skin extract based on one Example of this invention. It is the graph which showed the IL-8 secretion decreasing effect by the trypsin and active peptide (SLIGKV) of a chestnut skin extract based on one Example of this invention. It is the graph which showed the GM-CSF secretion reduction effect by the trypsin and active peptide (SLIGKV) of a chestnut skin extract based on one Example of this invention. It is the graph which showed the pruritus suppression effect with respect to the atopic dermatitis patient of the chestnut skin extract based on one Example of this invention. It is the graph which showed the measurement result of the PAR-2 activity inhibitory effect by the inner skin (astringent skin) and the outer skin (devil skin) extract of chestnut based on one Example of this invention.

  The present invention relates to a cosmetic composition for alleviating or suppressing pruritus comprising a chestnut skin extract as an active ingredient. The inventors of the present application measured the degree of PAR-2 activity suppression by chestnut skin extract using proteolytic enzyme active receptor-2 (PAR-2) as a target for treatment of pruritus, and the results will be described later. As demonstrated in the examples, it was confirmed that it showed excellent PAR-2 antagonism in vitro, and that it has a itch suppression effect on patients suffering from atopic dermatitis. confirmed.

  The pruritus is also referred to as pruritus, and the cause or form of such pruritus is not particularly limited, but for example, inflammatory dermatitis, atopic dermatitis, dermatitis due to rough skin, ash, itching, frostbite, It may be induced from one or more of dermatitis consisting of contact dermatitis, seborrheic dermatitis, psoriasis and psoriasis.

  Moreover, this invention contains a chestnut skin extract as an active ingredient, and shows the skin barrier function improvement effect. Thereby, the secondary skin damage induced by the disease or itching caused by the decrease in the skin barrier function can be effectively prevented or treated.

  The composition has a significant effect on reducing skin barrier damage or improving skin barrier resilience, for example, against secondary skin damage caused by itching resulting from atopic dermatitis. Can improve the skin barrier.

  The composition can improve the skin barrier especially through enhancement of skin moisturization and prevention of skin hyperkeratinization, and the inventors of the present application have found nothing as demonstrated through the examples described later. Experiments were carried out with an allergy model in which hair mice were treated with oxazolone, and transdermal water loss (TEWL) and skin thickness were measured. It was confirmed that the moisture retention enhancement or hyperkeratinization prevention effect was exhibited.

  Furthermore, this invention relates to the cosmetics composition for immunosuppression which contains a chestnut skin extract as an active ingredient. The composition may be, for example, a composition for the treatment of atopy, rheumatoid arthritis or Crohn's disease, among which a composition for the prevention or treatment of atopic disease which is an immune hypersensitivity reaction It can be a thing.

  When an atopic disease develops from an acute stage to a chronic disease stage due to skin damage, etc., various secretory changes in immune mediators are observed, but a number of intermediaries are observed in the damaged skin of patients suffering from atopic disease. The concentration of leukin will increase. In addition, granulocyte macrophage colony stimulating factor (GM-CSF) is known to increase in the amount of secretion in damaged skin of patients with atopic skin disease and cause a chronic inflammatory response. (Matsubara et al., FEBS Letters, 566, pp195-200, 2004).

  In this context, the inventors of the present application have found that the chestnut skin extract is associated with an immune hypersensitivity reaction, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1α. When it was confirmed that the expression of (IL-1α), interleukin-8 (IL-8) or granulocyte macrophage colony stimulating factor (GM-CSF) can be significantly reduced, chestnut extract is immunosuppressive. Suitable for active ingredients of cosmetic compositions.

In particular, the present invention contains a chestnut skin extract as an active ingredient, and is suitable as an active ingredient of a cosmetic composition for improving or treating atopic dermatitis.
Moreover, the said interleukin-6 (IL-6) and interleukin-8 (IL-8) are also known as a factor which induces itching in an atopic disease, and a chestnut skin extract is an itchy derived from an atopic disease. It can be effectively used for the prevention and treatment of symptoms.

  The chestnut skin means dark brown skin covering chestnut fruit, and the chestnut skin extract used in the present specification is selected from the group consisting of chestnut endothelium (astringent skin), outer skin and a mixture thereof. May mean one or more extracted extracts. As chestnut skin, chestnut endothelium (astringent skin) can be used, and chestnut skin (demon skin) may be used, but it is particularly excellent in the group treated with chestnut skin (demon skin) extract. PAR-2 antagonistic activity was confirmed.

  The chestnut skin may be any skin derived from any kind of chestnut, and is not particularly limited. For example, chestnut (Castana crenata S. et Z., Castanea molissima Bl., Castanea bulgaris) ) And one or more chestnut skins selected from the group consisting of Korean chestnuts (Castana crenat for. Multicarpa (Uyeki) Chung).

  The method for extracting the chestnut skin extract is not particularly limited. For example, the chestnut skin extract is extracted through a solvent selected from the group consisting of water, a lower alcohol having 1 to 4 carbon atoms, 1,3-butylene glycol, and a mixed solvent thereof. For example, the solvent may be one or more selected from the group consisting of water, methanol, ethanol, 1,3-butylene glycol, butanol, and mixtures thereof. Preferably, the chestnut extract is It may be extracted from 10-100% alcohol aqueous solution or 10-100% 1,3-butylene glycol, specifically, chestnut skin 20-90% ethanol aqueous extract or 10-70% 1,3-butylene glycol extract More specifically, chestnut skin 40-90% aqueous ethanol extract or 10-50% 1,3-butylene glycol extraction May be in, may be more specifically, 60% to 90% bark chestnut aqueous ethanol extract or 20-40% 1,3-butylene glycol extract.

  The content of the chestnut skin extract contained in the composition is not particularly limited, but may be contained in a content of 0.005 to 80% by weight, preferably 0.01 to 30% by weight based on the total weight of the composition. % May be included. If the content of the chestnut skin extract is too small, the effect becomes insignificant, and if it is too large, the stability of the dosage form may be lowered.

  In some cases, it is also possible to combine chestnut skin extract with one or more of antihistamines, steroids, local anesthetics, and immunosuppressive agents for alleviating or suppressing pruritus and immunosuppression.

  Traditionally, the technology for alleviating atopic dermatitis and pruritus has been to take antihistamines and apply steroid preparations as external preparations. In the case of these preparations, even if they show temporary therapeutic effects, It has the disadvantage of recurrence, and side effects such as central nervous system disorders and gastrointestinal disorders have been reported when these drugs are taken. A corticosteroid, a steroid preparation, has excellent anti-inflammatory and immunosuppressive effects, but side effects are also serious, and the immunosuppressive agent tacrolimus hydrate ointment is effective in treating atopic dermatitis However, it may be difficult to use for a long time in terms of safety, because it may induce skin cancer or kidney damage when it is absorbed into the skin damage site. It is a fact.

  Therefore, when appropriately using one or more of a composition containing chestnut skin extract as an active ingredient and one or more of antihistamine, steroid, local anesthesia, and immunosuppressive agent, alleviation or suppression of itching, immunosuppression, etc. Can have a large effect safely without side effects.

  The dosage form of the cosmetic composition is not particularly limited, and a cosmetic dosage form may be appropriately selected according to the purpose. For example, soft lotion (skin lotion and milk lotion), nutrition lotion, essence, nutrition cream, massage cream, pack, gel, eye cream, eye essence, cleansing cream, cleansing foam, cleansing water, powder, body lotion, body It can be formulated into one or more selected from the group consisting of cream, body oil, and body essence, but is not necessarily limited thereto.

  Determination of the dosage of the active ingredient is at the level of those skilled in the art, and the daily dosage of the composition depends on various factors such as the degree of progression of the subject to be administered, the time of onset, age, health condition, complications, etc. Depending on the adult, the composition is generally 1 to 500 mg / kg, preferably 30 to 200 mg / kg divided into 1 to 2 times per day. The amount is not intended to limit the scope of the invention in any way.

Hereinafter, the present invention will be described in more detail through examples. However, the following examples are for illustrating the present invention, and the category of the present invention is not limited to these examples.
[Example 1] Manufacture of chestnut skin extract 1-1) Manufacture of chestnut skin 1,3-butylene glycol extract Chestnut skin was obtained using 30% 1,3-butylene glycol (1,3-butylene glycol). And leached for 3 days at room temperature. Then, it filtered sequentially with the filter of the magnitude | size of 250 mesh, 3 micrometers, 1 micrometer, and 0.5 micrometer. Then, after leaving at 0-4 degreeC for 3 days, it filtered sequentially with the filter of the magnitude | size of 0.5 micrometer, 0.3 micrometer, and 0.2 micrometer, and the chestnut skin 1, 3- butylene glycol extract was obtained.

1-2) Production of Chestnut Ethanol Extract Chestnut skin was leached for 3 days at room temperature using 70% ethanol. Then, it filtered sequentially with the filter of the magnitude | size of 250 mesh, 3 micrometers, 1 micrometer, 0.5 micrometer, 0.3 micrometer, and 0.2 micrometer. Then, after concentrating a solution at 60 degreeC, it vacuum-dried at 30 degreeC for 18 hours, and obtained the chestnut skin ethanol extract in the powder form.

[Test Example 1] Inhibitory effect of chestnut skin ethanol extract on PAR-2 activity (in vitro, trypsin treatment, HEK: human epidermal keratinocytes)
One day before the experiment, keratinocytes (cell line name: HaCaT, source: ATCC) were separated into 96-well plates at 4 × 10 ⁴ cells / well, and then 24 ° C. in a 37 ° C., 5% CO ₂ incubator. Incubate for hours. After 24 hours, the 96-well plate was washed twice with HBSS (Hanks' Balanced Salt solution) buffer, and then a reaction buffer (2 μM Fluo-4-AM, 20% pluronic acid, 2.5 mM probenecid) was added to the cells. After reacting at 37 ° C. in a 5% CO ₂ incubator for 30 minutes and at room temperature for 30 minutes, it was washed twice with HBSS buffer, and the chestnut ethanol extract was added to the cells at 1 ppm, 2 ppm, 5 ppm, 10 ppm, 20 ppm, 30 ppm and Treated at a concentration of 50 ppm. After reacting for 10 minutes, the cells were treated with 2 U / ml trypsin, and changes in intracellular Ca ²⁺ concentration were measured for 80 seconds. For measuring the intracellular Ca ²⁺ concentration change, FlexStation 3 (Molecular Device, USA) was used. After the chestnut skin ethanol extract and trypsin treatment, the difference between the minimum and maximum values obtained by measuring the flex for 80 seconds was determined, and then the values were calculated as the minimum and maximum values during trypsin treatment. The inhibition rate was calculated in comparison with the difference.

  Referring to FIG. 1, when PAR-2 is activated by trypsin cutting the serine sequence at the N-terminus of PAR-2, calcium ions are flowed into the cell, but the chestnut skin extract was processed. In the case of a group, it can be confirmed that PAR-2 activation is suppressed and the inflow of calcium ions is remarkably reduced.

[Test Example 2] PAR-2 activity inhibitory effect of chestnut skin ethanol extract (in vitro, SLIGKV treatment, HEK: human epidermal keratinocytes)
One day before the experiment, keratinocytes (cell line name: HaCaT, source: ATCC) were separated into 96-well plates at 4 × 10 ⁴ cells / well, and then 24 ° C. in a 37 ° C., 5% CO ₂ incubator. Incubate for hours. After 24 hours, the 96-well plate was washed twice with HBSS (Hanks' Balanced Salt solution) buffer, and then a reaction buffer (2 μM Fluo-4-AM, 20% pluronic acid, 2.5 mM probenecid) was added to the cells. After reacting at 37 ° C. in a 5% CO ₂ incubator for 30 minutes and at room temperature for 30 minutes, it was washed twice with HBSS buffer, and the chestnut ethanol extract was added to the cells at 1 ppm, 2 ppm, 5 ppm, 10 ppm, 20 ppm, 30 ppm and Treated at a concentration of 50 ppm. After reacting for 10 minutes, 5 μM PAR-AP (SLIGKV) was treated, and changes in intracellular Ca ²⁺ concentration were measured for 80 seconds. For measuring the intracellular Ca ²⁺ concentration change, FlexStation 3 (Molecular Device, USA) was used. After the chestnut skin ethanol extract and 5 μM PAR-AP (SLIGKV) treatment, the difference between the minimum value and the maximum value obtained by measuring the flex for 80 seconds was determined, and then the value was determined to be 5 μM PAR-AP. The inhibition rate was obtained by comparing with the difference between the minimum value and the maximum value during the (SLIGKV) treatment.

  Referring to FIG. 2, when SLIGKV (Human), an activation peptide, acts as a direct ligand and PAR-2 is activated, calcium ions are introduced into the cell. In the case of the treated group, it can be confirmed that PAR-2 activation is suppressed and the inflow of calcium ions is significantly reduced.

[Test Example 3] PAR-2 activity inhibitory effect of chestnut skin 1,3-butylene glycol (BG) extract (in vitro, SLIGKV treatment, HEK: human epidermal keratinocytes)
One day before the experiment, keratinocytes (cell line name: HaCaT, source: ATCC) were separated into 96-well plates at 4 × 10 ⁴ cells / well, and then 24 ° C. in a 37 ° C., 5% CO ₂ incubator. Incubate for hours. After 24 hours, the 96-well plate was washed twice with HBSS (Hanks' Balanced Salt solution) buffer, and then a reaction buffer (2 μM Fluo-4-AM, 20% pluronic acid, 2.5 mM probenecid) was added to the cells. After reacting at 37 ° C. in a 5% CO ₂ incubator for 30 minutes and at room temperature for 30 minutes, the cells were washed twice with HBSS buffer, and the chestnut skin 1,3-butylene glycol (BG) extract was added to each cell at 0.1 w / Treatment was performed at concentrations of v%, 0.5 w / v% and 1 w / v%. After reacting for 10 minutes, 2 U / ml trypsin or 5 μM PAR-AP (SLIGKV) was treated, and changes in intracellular Ca ²⁺ concentration were measured for 80 seconds. For measuring the intracellular Ca ²⁺ concentration change, FlexStation 3 (Molecular Device, USA) was used. After the treatment with chestnut skin 1,3-butylene glycol (BG) and 2 U / ml trypsin or 5 μM PAR-AP (SLIGKV), the minimum and maximum values obtained by measuring flex for 80 seconds After obtaining the difference, the inhibition rate was obtained by comparing the value with the difference between the minimum value and the maximum value when treated with 2 U / ml trypsin or 5 μM PAR-AP (SLIGKV).

  Referring to FIG. 3, it can be confirmed that the influx of intracellular calcium ions by trypsin or PAR-2 active peptide (SLIGKV) significantly decreases as the concentration of chestnut skin extract increases.

[Test Example 4] Decrease in TNF-α secretion by chestnut skin extract One day before the experiment, normal human epidermal keratinocytes (NHEK, source: Lonza) were placed in a 96-well plate at 5 × 10 ⁴ cells / well. After separation, the cells were cultured at 37 ° C. in a 5% CO ₂ incubator for 24 hours. After 24 hours, the cells were washed twice with PBS and replaced with serum-free KBM (keratinocyte basement media). Chestnut skin was treated for each well according to the concentration (10, 25, 50 ppm), reacted for 30 minutes, and then treated with PGSA (10, 50 ppm) and LPS (1 ppm). After culturing for 24 hours at 37 ° C. in a 5% CO ₂ incubator, the culture solution was taken out and subjected to ELISA for TNF-α. The ELISA utilized the experimental method of the manufacturing company (BD science).

Referring to FIG. 4, it can be observed that chestnut skin significantly reduces the secretion of TNF-α increased by PGSA and LPS.
[Test Example 5] Decrease in IL-6 secretion by chestnut skin extract Except that an ELISA for IL-6 was performed, the same method as in Test Example 4 was used.

Referring to FIG. 5, it can be observed that chestnut skin suppresses IL-6 secretion increased by PGSA and LPS.
[Test Example 6] Decrease in IL-1α secretion by chestnut skin extract Except that an ELISA for IL-1α was performed, the same method as in Test Example 4 was used.

Referring to FIG. 6, it can be observed that chestnut skin decreases the amount of IL-1α secretion increased by PGSA and LPS depending on the concentration.
[Test Example 7] Decrease in IL-8 secretion by chestnut skin extract Except that an ELISA for IL-8 was performed, the same method as in Test Example 4 was used.

Referring to FIG. 7, it can be observed that chestnut skin significantly reduces IL-8 secretion increased by PGSA and LPS.
[Test Example 8] Decrease in GM-CSF secretion by chestnut skin extract Except that an ELISA for GM-CSF was performed, the same method as in Test Example 4 was used.

Referring to FIG. 8, it can be observed that the amount of GM-CSF secreted by PGSA and LPS decreases as the concentration of chestnut skin increases.
[Test Example 9] IL-6 secretion inhibitory effect of trypsin and active peptide (SLIGKV) in chestnut skin extract One day before the experiment, normal human epidermal keratinocytes (NHEK, source: Lonza) were placed in a 96-well plate at 5 ×. After separating the cells to 10 ⁴ cells / well, the cells were cultured at 37 ° C. in a 5% CO ₂ incubator for 24 hours. After 24 hours, cells were washed twice with PBS and replaced with serum-free KBM. Each well was treated with a chestnut skin extract according to its concentration (10, 50 ppm), reacted for 30 minutes, and then treated with trypsin (10 nM) or PAR-2 activating peptide (SLIGKV, 50 μM). After culturing for 24 hours at 37 ° C. in a 5% CO ₂ incubator, the culture solution was taken out and subjected to ELISA for IL-6. The ELISA utilized the experimental method of the manufacturing company (BD science).

Referring to FIG. 9, it can be observed that chestnut skin extract suppresses IL-6 secretion by trypsin and active peptide (SLIGKV) in a concentration-dependent manner.
[Test Example 10] Secretory inhibitory effect of IL-8 by trypsin and active peptide (SLIGKV) of chestnut skin extract Except that an ELISA for IL-8 was performed, the same method as in Test Example 9 was used. .

Referring to FIG. 10, it can be observed that the chestnut skin extract suppresses IL-8 secretion by trypsin and active peptide (SLIGKV) in a concentration-dependent manner.
[Test Example 11] GM-CSF secretion inhibitory effect of trypsin and active peptide (SLIGKV) in chestnut skin extract The same method as in Test Example 9 was used except that ELISA was performed on GM-CSF. .

Referring to FIG. 11, it can be observed that chestnut skin extract suppresses GM-CSF secretion by trypsin and active peptide (SLIGKV) in a concentration-dependent manner.
[Test Example 12] Itching effect of chestnut skin extract for patients with atopic dermatitis About 2 weeks, chestnut skin extract (0.3% solid content) was scooped for 10 patients with atopic dermatitis After intensive use on the site, the degree of itchiness before and after use was measured on a 7-point questionnaire, and the itch reduction effect was confirmed.

Referring to FIG. 12, after the chestnut skin extract was used for 2 weeks, it was possible to observe that the degree of itchiness decreased by one point.
[Test Example 13] Measurement of skin moisturizing effect of chestnut skin ethanol extract About 2 weeks, 10 chestnut skin extracts (0.3% solids concentration) were concentrated on the scooping site for 10 patients with atopic dermatitis After use, the moisture level of the skin before and after use was measured with a 7-point scale questionnaire to confirm the skin moisturizing effect. As a result of confirming the score of 10 people, it was an average of 6 points, and it was observed that the skin responded when the skin was moistened after application of the extract and showed an excellent skin moisturizing effect.

[Test Example 14] Comparison of PAR-2 activity inhibitory effect of chestnut rind ethanol extract and chestnut endothelial ethanol extract (in vitro, SLIGKV treatment, HEK: human epidermal keratinocytes)
After separating and drying the chestnut hull and the endothelium, a chestnut hull extract was produced in the same manner as in Example 1-2), and the chestnut inner skin extract was also produced in the same manner as in Example 1-2). Manufactured. Using the same method as in Test Example 2, the PAR-2 activity inhibitory effect of chestnut skin ethanol extract and chestnut endothelial ethanol extract was measured and is shown in Table 6 and FIG.

[Test Example 15] Comparison of PAR-2 activity inhibitory effect of chestnut rind ethanol extract and chestnut endothelial ethanol extract (in vitro, SLIGKV treatment, HEK: human epidermal keratinocytes)
The inhibitory effect of PAR-2 activity was measured by the same method as in Test Example 14 except that the concentrations of chestnut skin (demon skin) and endothelium (astringent skin) extract were processed as shown in Table 7 below.

Hereinafter, examples of dosage forms of the composition according to the present invention will be described. However, the cosmetic composition can be applied to various dosage forms, and this is not intended to limit the present invention. I will try to explain it.

[Form example 1] Soft lotion (skin lotion)
According to the composition described in Table 1 below, a soft lotion was produced by an ordinary method.

[Form example 2] Nutrition lotion (milk lotion)
With the composition described in Table 2 below, a nutritive lotion was produced by a conventional method.

[Formulation Example 3] Nutritional Cream Nutritional cream was produced by the usual method according to the composition described in Table 3 below.

[Formulation Example 4] Massage Cream A massage cream was produced by the usual method according to the composition described in Table 4 below.

[Dosage Form Example 5] Pack With the composition described in Table 5 below, a pack was produced by a conventional method.

Claims (15)

  A cosmetic composition for reducing or suppressing pruritus, comprising chestnut skin extract as an active ingredient.   The composition is any one or more of dermatitis consisting of inflammatory dermatitis, atopic dermatitis, rough skin dermatitis, hot skin, drowning, frostbite, contact dermatitis, seborrheic dermatitis, psoriasis and psoriasis The cosmetic composition for alleviating or inhibiting pruritus according to claim 1, wherein the pruritus induced by pruritus is alleviated or inhibited.   The cosmetic composition for alleviating or suppressing pruritus according to claim 1, wherein the composition alleviates or inhibits pruritus induced by atopic dermatitis.   A cosmetic composition for improving skin barrier function, comprising chestnut skin extract as an active ingredient.   The cosmetic composition for improving a skin barrier according to claim 4, wherein the composition is for alleviating skin barrier damage derived from atopic dermatitis or improving the resilience of the skin barrier.   The cosmetic composition for improving a skin barrier according to claim 4, wherein the composition is for enhancing skin moisture retention or preventing skin hyperkeratinization.   A cosmetic composition for immunosuppression comprising chestnut skin extract as an active ingredient.   The cosmetic composition for immunosuppression according to claim 7, wherein the composition is for the prevention or treatment of atopic disease.   The cosmetic composition for immunosuppression according to claim 7, wherein the composition is for the treatment of atopy.   A cosmetic composition for improving or treating atopic dermatitis, comprising chestnut skin extract as an active ingredient.   The cosmetic composition according to any one of claims 1 to 10, wherein the chestnut skin extract is contained in a content of 0.005 to 80% by weight based on the total weight of the composition.   The cosmetic composition according to any one of claims 1 to 10, wherein the chestnut skin is one or more selected from the group consisting of chestnut inner skin, outer skin, and a mixture thereof.   The cosmetic composition according to claim 12, wherein the chestnut skin is a chestnut skin (demon skin).   The chestnut skin extract is extracted through one or more solvents selected from water, lower alcohols having 1 to 4 carbon atoms, 1,3-butylene glycol, and mixed solvents thereof. The cosmetic composition according to any one of the above.   The cosmetic composition according to claim 14, wherein the chestnut skin extract is extracted through a solvent selected from the group consisting of water, methanol, ethanol, butanol, 1,3-butylene glycol, and a mixture thereof. .