CN105662905A - Application of dihydromyricetin in preparation of skin-care products or drugs for preventing and treating optical skin injuries - Google Patents

Abstract

The invention belongs to the field of medicine and cosmetics and discloses application of dihydromyricetin in the preparation of skin-care products or drugs for preventing and treating optical skin injuries.The skin-care product prepared from dihydromyricetin for preventing and treating optical skin injuries is sun screen, wherein the sun screen comprises: water, propylene glycol, glycerol, trehalose, oat beta-glucan, dihydromyricetin, C20-22 alkyl phosphate, polydimethylsiloxane, isononyl isononanoate and methylparaben.Experiments with a UVA induced HaCaT cell model proves that dihydromyricetin is effective in inhibiting cell ROS generation, reducing expression of apoptosis factors and inflammatory factors, reliving oxidization damage to cells, reducing inflammatory reaction of cells and cell apoptosis and preventing and treating optical skin injuries.The dihydromyricetin has a promising development prospect in the preparation of skin-care products or drugs for preventing and treating optical skin injuries.

Description

The purposes of dibydro myricetrin in preparation control dermal photodamage skin care product or medicine

Technical field

The invention belongs to medical cosmetic field, it is specifically related to the purposes of dibydro myricetrin in preparation control dermal photodamage skin care product or medicine.

Background technology

Along with atmospheric ozone layer suffers day by day serious destruction, ultraviolet radiation intensity strengthens, and standard of living improves gradually, and outdoor activity, the chance of light bath increases, and causes people to accept too much uviolizing, and light damaging tetter increases gradually. Ultraviolet can be divided into long wave ultraviolet (UVA, 320-400nm) by its wavelength difference, ultraviolet B radiation (UVB, 280-320nm) and short wave ultraviolet (UVC, 200-280nm) three kinds. Wherein UVC is almost all absorbed by the ozone in air stratosphere, mainly UVA and UVB therefore worked by human body. Research in the past thinks that UVB has the energy stronger than UVA, therefore UVB is considered as causing the major cause of skin injury. But current research in recent years shows that UVA is causing also producing the impact that should not be underestimated in skin injury and photoaging. Because having accounted for 95-98% compared to content in ultraviolet radiation of UVB, UVA; And UVA has the penetrativity stronger than UVB, it is possible to through dermal layer of the skin; The mankind can produced radiation effect by last UVA throughout the year, and the radiation effect of UVB mainly concentrates on summer.

Causing the mechanism of photosensitivity tetter not fully aware of yet at present, but comparatively it is clear that its morbidity is relevant to inflammatory reaction, immune response and apoptosis etc., the onset relation with photosensitivity tetter of dying of wherein withering with keratinocyte again is the closest.

Keratinocyte (HaCaT) is the main cell forming epidermis, it is possible to protection body is from extraneous physics, and the infringement of chemistry and microorganism, maintains the stable of organismic internal environment. In addition modern study shows that keratinocyte also take part in various biological procedures such as immunity, inflammation, hyperplasia and tumor transformation etc. UVA can cause increasing of oxyradical after irradiating skin, causes the excessive generation of the ROS in skin.The a large amount of ROS produced in body can cause the unbalance of oxidation system and antioxidant system, oxide compound has little time removing and is deposited in body response to oxidative stress occurs, causing a large amount of releases of neutrophil leucocyte inflammatory infiltration and inflammatory factor, this is considered as causing disease and the old and feeble important factor occurred. On the other hand, excessive ROS can also by destroying cell DNA, and the activity of cell death inducing destructive enzyme, failure line plastochondria, causes its function to damage. In sum, the cell oxidative damage that ROS causes is the important mechanisms that UVA causes skin photoage. Therefore in order to protect keratinocyte, safeguarding its normal function, alleviating the oxidative damage that ultraviolet causes is an important aspect.

The extract that dibydro myricetrin (Dihydromyricelin, DHM or DMY) is vitis spp vine tea is main active ingredient flavonoid compound in vine tea, and molecular formula is C₁₅H₁₂O₈. Modern pharmacology research shows, DHM has scavenging free radicals, anti-oxidant, anti-inflammation, antithrombotic, and antitumor, step-down, to fall the various biological such as fat, analgesia active. Up to now, DHM is not had to have the relevant report of the skin injury caused effect of uv-resistant A.

Summary of the invention

In order to overcome the deficiencies in the prior art, it is an object of the invention to provide the purposes of dibydro myricetrin in preparation control dermal photodamage skin care product or medicine.

The technical scheme that the present invention solves the problems of the technologies described above is as follows:

The purposes of the dibydro myricetrin of the present invention in preparation control dermal photodamage product, described product is skin care product or medicine.

Further, described skin care product are face cleaning milk, emulsion, essence, toner, face cream, facial mask, sun screen or stoste.

Further, described medicine is powder, granule, tablet, capsule, pill, oral liquid, injection, powder injection or ointment.

Further, skin care product of the present invention are sun screen.

Further, described sun screen is made up of the component of following per-cent meter: propylene glycol 2-6%, glycerine 2-6%, trehalose 2-4%, avenabeta glucosan 2-4%, dibydro myricetrin 2-6%, C_20-22Alcohol phosphoric acid ester 1-4%, polydimethylsiloxane 1-4%, isononyl isononanoate 1-4%, methyl hydroxybenzoate 0.1-0.2%, surplus is water.

Preferably, described sun screen is made up of the component of following per-cent meter: propylene glycol 4%, glycerine 4%, trehalose 4%, avenabeta glucosan 4%, dibydro myricetrin 6%, C_20-22Alcohol phosphoric acid ester 4%, polydimethylsiloxane 3%, isononyl isononanoate 3%, methyl hydroxybenzoate 0.1%, surplus is water.

Correspondingly, the preparation method of described sun screen, comprises the following steps:

S1: get dibydro myricetrin, propylene glycol, glycerine, trehalose and water and be placed in emulsification pot, be heated to 75-80 DEG C, stirs evenly, obtains material A;

S2: get C_20-22Alcohol phosphoric acid ester, polydimethylsiloxane and isononyl isononanoate are placed in oil cauldron, are heated to 75-80 DEG C, stir evenly, obtain material B;

S3: described material B is joined in the emulsification pot of S1 and stir with material A, homogeneous 10-15min, cooling;

S4: be cooled to 40 DEG C, adds avenabeta glucosan and methyl hydroxybenzoate, stirs, and cooling, obtains sun screen.

In addition, request of the present invention protection prevents and treats the purposes in dermal photodamage skin care product or medicine containing the composition of dibydro myricetrin in preparation.

The present invention induces the test of HaCaT cell model by UVA, proves DHM can improve UVA irradiation after the survival rate of HaCaT cell, make the minimizing of dying of withering of HaCaT cell, and reduce the expression of inflammatory factor.Described DHM generates by reducing the ROS of the HaCaT cell that UVA causes, and the proliferation activity of Cell protection, alleviates oxidative damage, and damages the ROS-MAPKs-NF-κ B path of HaCaT cell by intervening UVA, thus reduces the expression of inflammatory factor; In addition, DHM is by reducing the excessive generation of ROS, and on regulation and control mitochondrial membrane, Bcl-2 family protein is expressed, and recovers mitochondrial membrane potential, reduces the cracking activation of caspases and PARP, suppresses the apoptosis caused by UVA, reach the effect of control dermal photodamage.

The purposes of the dibydro myricetrin of the present invention in preparation control dermal photodamage skin care product or medicine, compared with prior art, has following advantage:

(1) dibydro myricetrin is the extract of vitis spp vine tea, and the content in vine tea can, up to 30%, be pure natural components, and source is abundant, it is easy to obtain and safe and non-stimulating;

(2) dibydro myricetrin can suppress UVA to induce HaCaT cell ROS to generate effectively, alleviate oxidative damage, reduce the expression of inflammatory factor, antiapoptotic factors, inhibited apoptosis, reach the effect of control dermal photodamage, can be widely used in preventing and treating in the skin care product of dermal photodamage or medicine;

(3) clinical trial shows, sun screen containing dibydro myricetrin can reduce the incidence of the malaise symptoms such as light injury patient skin itch, redness, pain significantly, and the generation of erythema after can effectively resisting illumination, for dermal photodamage, there is good preventive and therapeutic effect, it is applicable to prolonged application in antagonism dermal photodamage.

Accompanying drawing explanation

Fig. 1 is the cell survival rate of the HaCaT cell of different UVA dose irradiation;

Fig. 2 be DHM effect 6h after on the impact of cell survival rate of the HaCaT cell that UVA irradiates;

The impact of HaCaT intracellular ROS level that UVA is irradiated after being DHM effect 6h by Fig. 3;

The HaCaT intracellular cytokine Cox-2 that UVA is irradiated after being DHM effect 6h by Fig. 4, IL-1 β, the impact of IL-6 gene expression dose;

The HaCaT intracellular cytokine Bax that UVA is irradiated after being DHM effect 6h by Fig. 5, the change of Bcl-2 gene expression dose.

Embodiment

It will be understood by those skilled in the art that, technology disclosed in following examples represents the technology playing good action in the practice of the invention that the present inventor finds. But, disclosed specific embodiments can be made many changes, and still obtain same or similar result, and not depart from the spirit and scope of the present invention.

The impact of the cell survival rate of the HaCaT cell that UVA is irradiated by embodiment 1DHM

1. solution preparation

(1) preparation of DHM: the dibydro myricetrin powder getting 2.1mg is dissolved in 65.6 μ LDMSO (final volume of DMSO does not surpass 0.1%), is mixed with the storing solution of 100mmol/L, is stored in the PCR pipe of 200 μ L with 10 μ L/ pipes, keeps in Dark Place at-20 DEG C of refrigerators. Take out in advance during use, experimentally the needs of different concns, it may also be useful to DMEM is diluted to respective concentration.

(2) HaCaT cell culture medium (perfect medium): DMEM substratum (high sugar serum free medium)+10%FBS(South America foetal calf serum), its ratio is 9:1; Substratum adds dual anti-(penicillin and Streptomycin sulphate) so that it is final concentration is 100mg/L; Sealing film sealing, 4 DEG C save backup.

2. experimental technique

2.1 various dose UVA irradiate the survival impact of HaCaT cell

(1) cell collecting logarithmic phase growth is according to 1x10⁵The cell density of cells/ml is inoculated in 96 orifice plates, and 100 μ L are inoculated in every hole, and often group arranges 10 experimental ports, arranges cell controls group, 5%CO simultaneously₂, hatch for 37 DEG C.

(2) cultivating 24h, after cell grows to individual layer, inhale and abandon substratum and add PBS to covering cell, the UVA that experimental group gives 7.5min, 15min, 30min, 60min, 90min, 120min, 150min respectively irradiates;

(3) after irradiation, every hole continues to cultivate after adding 100 μ l perfect mediums, and 24h after illumination adds 10 μ LMTT solution in every hole, continues cultivation 4h;

(4) terminating cultivating, suck nutrient solution in hole carefully, 96 orifice plates are placed on shaking table after adding 100 μ L dimethyl sulfoxide (DMSO) low-speed oscillation 15min by every hole, and crystallisate is fully dissolved. Microplate reader is used to measure the light absorption value in each hole when the wavelength of 490nm.

(5) survival rate of each group of UVA radiation is calculated: cell survival rate (%)=(OD_{Experimental group}-OD_{Blank well})/(OD_{Cell controls group}-OD_{Blank well})×100%

The impact of the HaCaT cell survival that UVA is irradiated by 2.2DHM

(1) cell collecting logarithmic phase growth is according to 1x10⁵The cell density of cells/ml is inoculated in 96 orifice plates, and 100 μ L are inoculated in every hole, arrange cell controls group simultaneously. Often organize and 4 experimental ports are all set. Hatch for 5%CO2,37 DEG C.

(2) after cultivation 24h, cell grows to individual layer, and the DHM(concentration adding different concns in experimental group is set to 30 μm of ol/L, 20 μm of ol/L, 10 μm of ol/L, 5 μm of ol/L, 1 μm of ol/L, 0.5 μm of ol/L, 0.1 μm of ol/L, 0 μm of ol/L) and continue to cultivate 6h. Inhale after 6h and abandon substratum and add PBS to covering cell, give UVA and irradiate 60min;

(3) irradiated after inhale abandon PBS and recover irradiate before drug treating and continue to hatch 24h;

(4) UVA irradiate after 24h in every hole, add 10 μ LMTT solution, continue cultivate 4h;

(5) terminate cultivating, carefully suck the substratum in hole. 96 orifice plates are placed on shaking table after adding 100 μ L dimethyl sulfoxide (DMSO) low-speed oscillation 15min by every hole, and crystallisate is fully dissolved. Microplate reader is used to measure the light absorption value in each hole when the wavelength of 490nm. Cell survival rate (%)=(OD_{Experimental group}-OD_{Blank well})/(OD_{Cell controls group}-OD_{Blank well})×100%

3. data processing

Data all represent with mean+SD, adopt Student ' st-test to analyze, and P < 0.05 represents that data have significant difference, and P < 0.01 represents that data have pole significant difference.

4. experimental result

The survival condition of the HaCaT cell that 4.1 various dose UVA irradiate

Result is as shown in Figure 1. Mtt assay determination data shows, and along with the survival rate of the increase HaCaT cell of UVA exposure intensity declines gradually, presents certain dose relationship. And at 10J/cm²Time cell survival rate drop to about 50%, therefore we choose 10J/cm²UVA intensity as the exposure intensity of subsequent experimental.

The impact of the HaCaT cell survival that UVA is irradiated by 4.2DHM

Result is as shown in Figure 2. When the concentration of DHM is when 1 μm of below ol/L, DHM does not increase significantly UVA(10J/cm²) irradiate after the survival rate of 24hHaCaT cell, but when the concentration of DHM can suppress the decline of survival rate of the HaCaT cell caused by UVA irradiation significantly when 1～30 μm of ol/L,And reach maximum effect when 10 μm of ol/L.

The impact of the HaCaT intracellular ROS level that UVA is irradiated by embodiment 2DHM

1. experimental technique

(1) DCFH-DA preparation: dilute DCFH-DA with serum-free medium so that it is final concentration is 10 μm of ol/L;

(2) by the HaCaT cell of logarithmic phase according to 1x10⁵The cell density of cells/ml is inoculated in 35mm Tissue Culture Dish, every ware 2ml;

(3) cultivate after 24h and abandon old nutrient solution, and add the substratum containing different concns DHM and continue to hatch 6h;

(4) after 6h, substratum suction is abandoned and change PBS into, then uv irradiating 60min;

(5) uv irradiating changes PBS into substratum containing serum after terminating and continues to hatch 30min;

(6) after 30min, supernatant is abandoned in suction, adds the DCFH-DA diluted afterwards 3 times with PBS washed cell, and every ware 2ml also continues to hatch 30min at 37 DEG C;

(7) after 30min, supernatant is abandoned in suction, after PBS washed cell 3 times, adopts Laser Scanning Confocal Microscope detection ROS fluorescence intensity, and 488nm is as excitation wavelength, and 568nm is as emission wavelength.

2. data processing

Data all represent with mean+SD, adopt Student ' st-test to analyze, and P < 0.05 represents that data have significant difference, and P < 0.01 represents that data have pole significant difference.

3. experimental result

Result is as shown in Figure 3. Can find out that UVA generates a large amount of ROS in HaCaT cell after irradiating by the burnt result of copolymerization, and DHM can reduce uv-radiation significantly after the generation of ROS, but do not present certain dose-dependently.

The impact of inflammatory factor gene expression dose in the HaCaT cell that UVA is irradiated by embodiment 3DHM.

1. experimental technique

(1) cell collecting logarithmic phase growth is according to 1x10⁵The cell density of cells/ml is inoculated in the Tissue Culture Dish of 35mm, and every ware 2ml, is placed in 37 DEG C, 5%CO₂Cultivate in incubator;

(2) treat to abandon old nutrient solution after cell grows to individual layer after cultivation 24h, (concentration is 10 μm of ol/L to add the dibydro myricetrin of different concns in experimental group, 5 μm of ol/L, 2.5 μm of ol/L, 1.25 μm ol/L, 0 μm of ol/L), cell controls group continues to hatch 6h at 37 DEG C after adding the substratum containing serum, inhale after 6h and abandon substratum and add PBS to covering cell, then uv irradiating 60min, uv irradiating is inhaled after terminating and is abandoned PBS and again add the substratum containing serum, then continues to cultivate different time;

(3) 20min after uv irradiating, 40min, 60min, 80min, 100min receive cell and also extract total serum IgE according to Trizol method.

(4) Q-PCR is adopted to detect the change of inflammatory factor gene expression dose in different time cell.

2. data processing

Data all represent with mean+SD, adopt Student ' st-test to analyze, and P < 0.05 represents that data have significant difference, and P < 0.01 represents that data have pole significant difference.

3. experimental result

Result is as shown in Figure 4. Can find out that DHM can the expression that reduce inflammatory factor COX-2, IL-1, IL-6 caused by uv irradiation of concentration dependent by Q-PCR result.

The impact of antiapoptotic factors expression level in the HaCaT cell that UVA is irradiated by embodiment 4DHM.

1. experimental technique

(1) cell collecting logarithmic phase growth is according to 1x10⁵The cell density of cells/ml is inoculated in the Tissue Culture Dish of 35mm, and every ware 2ml, is placed in 37 DEG C, 5%CO₂Cultivate in incubator;

(2) treat to abandon old nutrient solution after cell grows to individual layer after cultivation 24h, the DHM(concentration adding different concns in experimental group is 10 μm of ol/L, 5 μm of ol/L, 2.5 μm of ol/L, 1.25 μm ol/L, 0 μm of ol/L), cell controls group continues to hatch 6h at 37 degree after adding the substratum containing serum, inhale after 6h and abandon substratum and add PBS to covering cell, then uv irradiating 60min, uv irradiating is inhaled after terminating and is abandoned PBS and again add the substratum containing serum, then continues to cultivate different time;

(3) 2h after uv irradiating, 4h, 6h, 8h, 10h, 12h, 14h collecting cell also extracts total serum IgE according to Trizol method.

(4) Q-PCR is adopted to detect the change of antiapoptotic factors gene expression dose in different time cell.

2. data processing

Data all represent with mean+SD, adopt Student ' st-test to analyze, and P < 0.05 represents that data have significant difference, and P < 0.01 represents that data have pole significant difference.

3. experimental result

Result is as shown in Figure 5. DHM can concentration dependent lower the rising of short apoptogene Bax caused by UVA irradiates, the expression pressing down apoptogene Bcl-2 can also be raised simultaneously.

The preparation of the anti-dermal photodamage sun screen of embodiment 5 the present invention

The sun screen of the anti-dermal photodamage of the present invention is made up of the component of following per-cent meter: propylene glycol 4%, glycerine 4%, trehalose 4%, avenabeta glucosan 4%, dibydro myricetrin 6%, C_20-22Alcohol phosphoric acid ester 4%, polydimethylsiloxane 3%, isononyl isononanoate 3%, methyl hydroxybenzoate 0.1%, surplus is water.

Preparation method:

S1: get dibydro myricetrin, propylene glycol, glycerine, trehalose and water and be placed in emulsification pot, be heated to 80 DEG C, stirs evenly, obtains material A;

S2: get C_20-22Alcohol phosphoric acid ester, polydimethylsiloxane and isononyl isononanoate are placed in oil cauldron, are heated to 80 DEG C, stir evenly, obtain material B;

S3: described material B is joined in the emulsification pot of S1 and stir with material A, homogeneous 15min, cooling;

S4: be cooled to 40 DEG C, adds avenabeta glucosan and methyl hydroxybenzoate, stirs, and cooling, obtains sun screen.

The preparation of the anti-dermal photodamage sun screen of embodiment 6 the present invention

The sun screen of the anti-dermal photodamage of the present invention is made up of the component of following per-cent meter: propylene glycol 2%, glycerine 2%, trehalose 2%, avenabeta glucosan 2%, dibydro myricetrin 2%, C_20-22Alcohol phosphoric acid ester 1%, polydimethylsiloxane 1%, isononyl isononanoate 1%, methyl hydroxybenzoate 0.1%, surplus is water.

Preparation method is with embodiment 5.

The preparation of the anti-dermal photodamage sun screen of embodiment 7 the present invention

The sun screen of the anti-dermal photodamage of the present invention is made up of the component of following per-cent meter: propylene glycol 6%, glycerine 6%, trehalose 4%, avenabeta glucosan 4%, dibydro myricetrin 6%, C_20-22Alcohol phosphoric acid ester 4%, polydimethylsiloxane 4%, isononyl isononanoate 4%, methyl hydroxybenzoate 0.2%, surplus is water.

Preparation method is with embodiment 5.

All meet the pertinent regulations requirement of QB/T1857-2013 through inspection embodiment 5 ~ 7 product, sense index (color and luster, fragrance, structure) meets industry regulation, and physical and chemical index (pH, heat-resisting, cold-resistant, actives) meets industry regulation.

Test example one, the present invention's anti-dermal photodamage sun screen Product Safety evaluate (human body skin spot is sturdy to be tested)

1. the anti-dermal photodamage sun screen that test drug: embodiment 5-7 prepares.

2. subjects and grouping: 240 example skin healths, without the tested volunteer of women of tetter allergies, 25-55 year, 34 years old mean age, be divided into 3 groups at random, often organize 80 people.

3. test method: select qualified spot examination device, experiment method is pasted with closed spot, the tested material getting about soya bean size is placed in spot examination device, external application special adhesive tape is covered on experimenter back, tested material is removed after 24 hours, within after removing respectively 2,4,6,12,24,48 hours, observe skin reaction, according to its result of skin reaction grade scale record in " cosmetics health specification ".

4. test-results: human skin patch result shows: each group experimenter is by the patch test of the antianaphylaxis toner of embodiment 5 ~ 7, skin reaction is observed at 2,4,6,12,24,48 hours, all without skin adverse reaction occurs, the sun screen use safety that the present invention obtains is described.

Test example two, the present invention's anti-dermal photodamage clinical drug efficacy study of sun screen

1. subjects:

The patient of screening 320 example skin health is as research object, and all research subject's skin types are similar, and patient signs Informed Consent Form, participate in experiment voluntarily, get rid of the heart, liver, kidney serious disease patient, get rid of photosensitization patient, and research object compliance is good. Wherein man 120 example, female 200 example, the age 18-55 year, average 35 years old. Adopt random digits table that research object is divided into test A, B, C group and comparative example group, often organize 80 people. These patients are at equal no significant difference traditionally, and partner treatment, difference not statistically significant, has comparability.

2. test method:

Comparative example group adopts the red pomegranate sunscreen of commercially available Estee Lauder; The anti-dermal photodamage sun screen that test A, B, component C do not adopt embodiment 5-7 obtained. After trier's cleaning skin, get sun screen and evenly it is applied in surface, Dermal exposure position, the process of smearing is avoided enter eyes, four groups of patients are carrying out uviolizing simultaneously, wavelength 320-400nm, irradiating position for research object face, irradiation time is half an hour, compares four groups of patients and erythema, uncomfortable reaction generation situation occurs.

3. observation index:

Relatively there is uncomfortable situation about reacting in four groups of patient skins, and mainly comprise itch, pain and redness, compare the situation that erythema occur in four groups of patient skins, are respectively without erythema, light red spot and obvious erythema. Obvious erythema is erythema area > 2cm, light red spot is erythema area 1-2cm, it is erythema area < 1cm without erythema, erythema is assessed by same evaluator, assess according to patient's different situations, light red spot is visible a small amount of erythema and paler colour, and obvious erythema refers to that erythema area is big and color is dark.

4. test-results

Table 1 is respectively organized the situation that patient skin is not suitable with generation and is compared

The comparison that erythema situation occurs in patient skin respectively organized by table 2

Dermal photodamage, mainly owing to action of ultraviolet radiation is in skin, destroys skin surface stratum corneum, and emergency reaction occurs in cell, finally causes the itch of skin surface, redness, heat pain, forms erythema, even destroy skin integrity. Commercially available commercially available Estee Lauder red pomegranate sunscreen contains the compositions such as red pomegranate elite, green tea extractive liquor, VITAMIN, titanium dioxide, have sun-proof, isolation, moisturizing effect, the present invention with the use of the red pomegranate sunscreen of Estee Lauder as a comparison case, investigates the effect of the present invention containing the anti-dermal photodamage of sun screen of dibydro myricetrin.

From upper table 1, four groups of patients are after illumination is penetrated, the skin of test A, B, C group is not suitable with incidence and is respectively 2.5%, 3.75%, 3.75%, is significantly lower than control group and is not suitable with incidence 8.75%, is wherein not suitable with incidence with the skin testing A group and embodiment 5 obtains sun screen minimum; By upper table 2 it will be seen that the skin erythema of test A, B, C group is not suitable with incidence and is respectively 2.5%, 3.75%, 3.75%, be significantly lower than control group and be not suitable with incidence 10%, wherein with test A group and embodiment 5 to obtain the skin erythema incidence of sun screen minimum. Above result shows, dibydro myricetrin can obviously reduce the incidence of the malaise symptoms such as patient skin itch, redness, pain, can effectively resist the generation of erythema after illumination, for dermal photodamage, there is good preventive and therapeutic effect, and effect with the obtained sun screen of embodiment 5 is best.

Above-described embodiment is the principle of illustrative the present invention and effect thereof only, but not for limiting the present invention. Above-described embodiment all under the spirit not running counter to the present invention and category, can be modified or change by any person skilled in the art scholar. Therefore, in art, tool usually intellectual, not departing under disclosed spirit and technological thought all the equivalence modifications completed or change, must be contained by the claim of the present invention such as.

Claims (9)

1. dibydro myricetrin prevents and treats the purposes in dermal photodamage skin care product or medicine in preparation.

2. the composition containing dibydro myricetrin prevents and treats the purposes in dermal photodamage skin care product or medicine in preparation.

3. purposes as claimed in claim 1 or 2, it is characterised in that, described skin care product be face cleaning milk, emulsion, essence,

Toner, face cream, facial mask, sun screen or stoste.

4. purposes as claimed in claim 1 or 2, it is characterised in that, described medicine is powder, granule, tablet, capsule

Agent, pill, oral liquid, injection, powder injection or ointment.

5. one kind contains the sun screen of the control dermal photodamage of dibydro myricetrin.

6. the sun screen of control dermal photodamage as claimed in claim 5, it is characterised in that, described sun screen is made up of the component of following per-cent meter: propylene glycol 2-6%, glycerine 2-6%, trehalose 2-4%, avenabeta glucosan 2-4%, dibydro myricetrin 2-6%, C_20-22Alcohol phosphoric acid ester 1-4%, polydimethylsiloxane 1-4%, isononyl isononanoate 1-4%, methyl hydroxybenzoate 0.1-0.2%, surplus is water.

7. the sun screen of control dermal photodamage as claimed in claim 5, it is characterised in that, described sun screen is made up of the component of following per-cent meter: propylene glycol 4%, glycerine 4%, trehalose 4%, avenabeta glucosan 4%, dibydro myricetrin 6%, C_20-22Alcohol phosphoric acid ester 4%, polydimethylsiloxane 3%, isononyl isononanoate 3%, methyl hydroxybenzoate 0.1%, surplus is water.

8. the sun screen of control dermal photodamage as claimed in claim 5, it is characterised in that, the preparation method of described sun screen comprises the following steps:

S1: get dibydro myricetrin, propylene glycol, glycerine, trehalose and water and be placed in emulsification pot, be heated to 75-80 DEG C, stirs evenly, obtains material A;

S2: get C_20-22Alcohol phosphoric acid ester, polydimethylsiloxane and isononyl isononanoate are placed in oil cauldron, are heated to 75-80 DEG C, stir evenly, obtain material B;

S3: described material B is joined in the emulsification pot of S1 and stir with material A, homogeneous 10-15min, cooling;

S4: be cooled to 40 DEG C, adds avenabeta glucosan and methyl hydroxybenzoate, stirs, and cooling, obtains sun screen.

9. the preparation method of the sun screen of the control dermal photodamage as described in as arbitrary in claim 5-8, it is characterised in that, comprise the following steps:

S1: get dibydro myricetrin, propylene glycol, glycerine, trehalose and water and be placed in emulsification pot, be heated to 75-80 DEG C, stirs evenly, obtains material A;

S2: get C_20-22Alcohol phosphoric acid ester, polydimethylsiloxane and isononyl isononanoate are placed in oil cauldron, are heated to 75-80 DEG C, stir evenly, obtain material B;

S3: described material B is joined in the emulsification pot of S1 and stir with material A, homogeneous 10-15min, cooling;

S4: be cooled to 40 DEG C, adds avenabeta glucosan and methyl hydroxybenzoate, stirs, and cooling, obtains sun screen.