CN109908161A - Application of the Ginsenoside compound K in preparation treatment atopic dermatitis external drug - Google Patents
Application of the Ginsenoside compound K in preparation treatment atopic dermatitis external drug Download PDFInfo
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Abstract
The present invention relates to field of medical technology, application of specifically a kind of Ginsenoside compound K in preparation treatment atopic dermatitis external drug and health & beauty products.The present invention polymerize gene deletion atopic dermatitis mouse by establishing OVA sensitization atopic dermatitis mouse model, choosing silk, and mouse is administered respectively with the Ginsenoside compound K of various concentration to obtain result: 1, Ginsenoside compound K can significantly reduce the AD model mice scratching frequency of OVA sensitization, reduce mouse skin and dermis thickness, middle concentration group and high concentration group is significant in efficacy is higher than low concentration group and Dexamethasone Cream group；2, Ginsenoside compound K can reduce the expression of IL-4 at the scoring of Ft mouse dermatitis and the scratching frequency and Ft mouse skin lesion, middle concentration group curative effect is higher than low concentration group and high concentration group, and Dexamethasone Cream causes the atopic dermatitis sample skin lesion of skin barrier function exception not have improvement result silk polymerization gene deletion.Product of the invention has the advantages that curative effect is good, safe.
Description
Technical field
The present invention relates to pharmaceutical technology fields, specifically, being Ginsenoside compound K in preparation treatment atopic dermatitis external application
Application in drug and makeup health care product.
Background technique
Atopic dermatitis (AtopicDermatitis, AD) is a kind of chronic, recurrent, inflammatory dermatoses, and patient is past
Toward will appear violent pruritis, quality of life is seriously affected.The usually initial hair patient before infancy, 1 years old of this disease accounts for about entirely
The 50% of portion patient, the disease are in chronic process, and some patientss state of an illness can delay adult, but the person that also has adult onset.It is sending out
It may be up to 10%~20% up to illness rate in national this sick child child.Over China, 20 years the illness rate of atopic dermatitis also by
Step rise, 1998 school age teenager (6~20 years old) total prevalence rate be 0.70%, 10 city preschool children in 2002
The illness rate of (1~7 years old) is 2.78%, and District of Shanghai epidemiological survey in 2012 is shown, child morbidity rate reaches within 3~6 years old
8.3% (male 8.5%, female 8.2%), city is significantly higher than rural area (10.2% to 4.6%).
The pathogenesis of atopic dermatitis is complex, it is now recognized that itself and immune, heredity, skin barrier function exception phase
It closes.Main expression Th2 cell associated cytokines (such as IL-4 and IL-13) and chemotactic in atopic dermatitis skin lesion because
Son, such as TARC (thymus gland and activated regulators).These chemotactic factor (CF)s have the Th2 cell of expression chemokine receptors CCR4
Chemotaxis.Therefore, Th2 cell usually is observed in cutaneous lesion, but this is the pathomechanism of AD acute stage, it was reported that produce
The Th1 cell of raw IFN-γ and IL-12 are in chronic phase dominance.
Langerhans cell and mast cell participate in inflammatory reaction by expressing a kind of IgE receptor of high-affinity, should be by
Body can cause antigen presenting cell and histamine release of mast cell, cell factor etc..Th2 cell factor IL-4 and IL-13 stimulation
Fibroblast generates periostin, and protein induced keratinocyte generates TSLP, and TSLP can induce Dendritic Cells production
The chemotactic factor (CF)s such as TARC/CCL17, to induce inflammatory reaction.Serum T ARC/CL17 level can be used as the short-term of atopic dermatitis
Disease marker, as a kind of new effector cell's Th17 cell relevant to allergic reaction, and for controlling overreaction
Treg (regulatory T cells) is also proved to related to AD.
The expression of ceramide and silk polymeric protein in atopic dermatitis patients skin lesion is reduced, it is considered to be barrier function
The main reason for obstacle.It is believed that the exception of barrier function is the secondary phenomenon with inflammation-related, it is also possible to idiocrasy
The cause of disease of dermatitis.Atopic dermatitis has research to be considered caused by reducing due to patient's itch threshold value with severe pruritus.According to report
Road, IL-31 are an important factor for causing AD patient's itch, it is generally recognized that antihistamine cannot control atopic dermatitis well
Caused itch.Histamine, Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 and its receptor play an important role in the itch of periphery.In recent years, endogenous opioids drug
As the effect of beta-endorphin and its receptor in central itch attracts attention.It is reported that morphine passes through GRP receptor-inducible scabies
Itch.
The clinical manifestation of atopic dermatitis is varied, it is most basic be characterized in dry skin, chronic eczema sample dermatitis and
Violent itch.This disease is most initial in infantile period, can partially betide children and adulthood.According to different age group
Performance, be divided into infancy, childhood and it is young with adulthood three phases.Infancy (birth was to 2 years old): it is wet to show as baby
Rash, is distributed in two cheeks, forehead and scalp more, and fash can be dried or be oozed out.Childhood (2~12 years old): mostly developed by infancy
, can also occur without infancy.It mostly occurs in the fossa cubitalis, rouge nest and shank and stretches side, be with subacute and chronic dermatitis
Main performance, fash is often dry plump, there is obvious lichenification.It is young with adulthood (12 years old or more): skin lesion and childhood
It is similar, also based on subacute and chronic dermatitis, occur mainly in the positions such as the fossa cubitalis, rouge nest, throat, can also betide trunk,
Four limbs, face, the back of the hand, most of in dry, hypertrophica dermatitis damage, some patientss can also appear as pruigo sample fash.
Atopic dermatitis is chronic relapsing disease, and the purpose for the treatment of is to alleviate or eliminate clinical symptoms, eliminate induce and/
Or Acute aggravated factors, it reduces and prevention is recurred, improve the quality of life of patient.Regular and good treatment can make atopic dermatitis
Symptom subsides or significantly improves completely, and patient can enjoy normal life.
Primary Care plays the part of important role in AD patient treats, and takes a shower and restores and skin barrier function is kept to seem
It is particularly important, patient should after shower external application moisturizer at once, and daily at least use 2 emollients.
In local external use's medication of AD patient, glucocorticoid and Calcineurin inhibitors are fiest-tire medications,
Glucocorticoid, which is used for a long time, can cause the adverse reaction of skin and system, such as local skin atrophy, blood capillary proliferation, thus
Some patientss feel misgivings to external application glucocorticoid.Calcineurin inhibitors are to the selective inhibition of T lymphocyte
Effect, has stronger anti-inflammatory effect, is chiefly used in neck surface and fold position.Adverse reaction is local irritation.
In the systemic agent of AD patient, it is preferred that antihistamine and anti-inflammatory medium drug, glucocorticoid and
Immunosuppressor.
Patients obvious for itch or with complication such as sleep disturbance, nettle rash, allergic rhinitises, can be selected first
Generation or second generation antihistamine, wherein first generation antihistamine facilitates patient's improvement itch and sleeps due to that can pass through blood-brain barrier
It sleeps.Other antiallergies and anti-inflammatory drug include thromboxane A2 inhibitor, leukotriene receptor antagonists, mast cell membrane stabilizer
Deng.
Use no or little glucocorticoid medicine as far as possible in principle.To the patient being in a bad way, other drugs are uncontrollable
Can short application use, should be reduced in time after sb.'s illness took a favorable turn, until be discontinued, for that hormone can be gradually transitions and exempted from compared with Refractory cases
Epidemic disease inhibitor or ultraviolet therapy.Prolonged application hormone should be avoided, to prevent the side effect of hormone, not mistake is reduced after Morbidity control
Fastly, subtract medicine or the too fast state of an illness that can lead to that is discontinued is bounced.
Immunosuppressor is suitable for being in a bad way and the uppity patient of routine treatment, at most with cyclosporine application, disease
It can decrescence as little as minimum maintenance after feelings control.Cyclosporine works very fast, but the state of an illness is easily repeatedly after being discontinued.It should be monitored during medication
Blood pressure and renal function suggest not carrying out phototherapy simultaneously during medication.Methotrexate (MTX) is common immunosuppressor, can be first from low dose
Start, blood picture is tightly monitored during medication, if having anaemia and oligoleukocythemia, should be discontinued immediately.
Ultraviolet light is the effective ways for treating atopic dermatitis, and narrow-band UVB and UVA1 are safe and effective, thus make
With most, it is also possible to traditional photochemotherapy, but it is noted that side effect.It should be noted that using emollient after phototherapy.6 years old or less youngsters
Child should be avoided using whole body ultraviolet therapy.
In conclusion the various treatment methods of AD have certain limitation at present, clinical treatment is usually combined a variety of
Therapy, but the state of an illness of AD is easy repeatedly, and the safely and effectively therapeutic agent of research and exploitation newly is significant.
Ginsenoside compound K (CK), entitled 20 (the S)-O- β-D- protopanoxadiol glucoside of chemistry are people
Join the active metabolite of saponin(e in vivo.Studies have shown that Ginsenoside compound K have it is antitumor, anti-inflammatory, resist myocardial ischemia
Reperfusion injury injures the multiple pharmacological effects such as protection chemical damage.In recent years, some scholars successively report ginseng both at home and abroad
Saponin(e CK all has certain inhibiting effect to including kinds of tumor cells such as hepatocellular carcinoma, nasopharyngeal carcinoma, colon cancer, bladder cancers,
But ginsenoside is rarely reported the research effect of atopic dermatitis.The present invention has studied Ginsenoside compound K for the first time can be used for preparing
Atopic dermatitis drug is treated, new therapeutic scheme is provided for atopic dermatitis disease, is had a good application prospect.
Summary of the invention
The first purpose of this invention is in view of the deficiencies of the prior art, it is special in preparation treatment to provide a kind of Ginsenoside compound K
Application in answering property dermatitis external drug.
Second object of the present invention is in view of the deficiencies of the prior art, it is special in preparation treatment to provide a kind of Ginsenoside compound K
Application in answering property dermatitis makeup health care product.
To realize above-mentioned first purpose, the technical solution adopted by the present invention is that:
Application of the Ginsenoside compound K in preparation treatment atopic dermatitis external drug.
Preferably, the Ginsenoside compound K shared parts by weight percentage in treatment atopic dermatitis external drug is 0.1-
99.9%.
Preferably, the treatment atopic dermatitis external drug is the excipient allowed by Ginsenoside compound K and external drug
Or carrier is made.
Preferably, the dosage form of the treatment atopic dermatitis external drug includes ointment, cream, liniment, spray
Mist agent and film.
To realize above-mentioned second purpose, the technical solution adopted by the present invention is that:
Application of the Ginsenoside compound K in the makeup health care product of preparation treatment atopic dermatitis, makeup health care product not only have office
The small modification in portion, and have Transdermal absorption, effect effect in external application, such as healthcare mist spray, creams.
Preferably, the Ginsenoside compound K shared parts by weight percentage in treatment atopic dermatitis makeup health care product is
0.1- 99.9%.
Preferably, the treatment atopic dermatitis makeup health care product is the tax allowed by Ginsenoside compound K and makeup health care product
Shape agent or carrier are made.
Preferably, the atopic dermatitis includes simple form and mixed type, the generally not concurrent Respiratory symptoms of simple form,
The respiratory hypersensitivities symptom such as asthma, allergic rhinitis generally can all occur in mixed type.
Preferably, the atopic dermatitis includes at least one symptom chosen from the followings: (1) pruritus；(2) it is rubescent and go out
Blood；(3) edema；(4) damage and tissue damage；(5) crust and drying are formed.
Ginsenoside compound K provided by the invention is for treating atopic dermatitis, and more existing common drug is (such as: sugared cortical hormone
Element) have significant advantage, outstanding behaviours be it is safe and effective, especially can integrally-regulated cellular immunity, efficacy stability after drug withdrawal.
And effective component is clear, can be made into the product forms of high quality, also has significant innovation and drug effect excellent with drug than existing methods
Gesture.
Ginsenoside compound K of the present invention belongs to protopanaxadiol-type's saponin(e, and the preparation method of Ginsenoside compound K includes changing
Method and bioanalysis: acid and alkali hydrolysis, microorganism conversion, enzymatic conversion and recombination enzymatic conversion.
The raw material of Ginsenoside compound K of the present invention includes: ginseng roots medicinal material, American Ginseng root medicinal material, gen-seng haulms
Medicinal material, stem and leaves of American ginseng medicinal material and their total extract or total saposins.
The invention has the advantages that:
1, it polymerize gene deletion mouse by establishing the AD model mice of OVA sensitization and choosing silk, respectively using different dense
Mouse is administered in the Ginsenoside compound K of degree, the results showed that (1) Ginsenoside compound K can significantly reduce the AD model mice of OVA sensitization
It scratches the frequency, reduce mouse skin and dermis thickness, middle concentration group and the high concentration group low concentration group significant in efficacy that is higher than are filled in ground
The loose emulsifiable paste group of rice；
(2) Ginsenoside compound K can reduce the expression of IL-4 at the scoring of Ft mouse dermatitis and the scratching frequency and Ft mouse skin lesion,
Middle concentration group curative effect is higher than low concentration group and high concentration group, and Dexamethasone Cream causes skin barrier for silk polymerization gene deletion
The atopic dermatitis sample skin lesion of dysfunction does not have improvement result.
2, the present invention indicates that Ginsenoside compound K is used to prepare the drug and makeup health care product for the treatment of atopic dermatitis for the first time,
With the prior art used in compared with drug such as glucocorticoid, Ginsenoside compound K has curative effect when treating atopic dermatitis
Low, the safer advantage of good, few side effects, recurrence rate, alleviates the pain of patient, has very strong practicability.
Detailed description of the invention
Attached drawing 1 is the mouse model flow chart of the percutaneous sensitization induction of ovalbumin antigen (OVA).
Attached drawing 2 is the mouse model each group dermatitis appraisal result statistical chart of the percutaneous sensitization induction of ovalbumin antigen (OVA).
Attached drawing 3 is the mouse model each group scratching frequency result statistical chart of the percutaneous sensitization induction of ovalbumin antigen (OVA).
Attached drawing 4 is the mouse model each group skin lesion pathologic condition dyeing knot of the percutaneous sensitization induction of ovalbumin antigen (OVA)
Fruit statistical chart.
Attached drawing 5 is the mouse model each group epidermal thickness result statistical chart of the percutaneous sensitization induction of ovalbumin antigen (OVA),
Note: model group ###P < 0.001 compared with normal group, each concentration C K group and Dexamethasone Cream group are compared with model group, * P <
0.05, * * P < 0.01, * * * P < 0.001.
Attached drawing 6 is the mouse model each group dermis thickness result statistical chart of the percutaneous sensitization induction of ovalbumin antigen (OVA),
Note: model group ###P < 0.001 compared with normal group, each concentration C K group and Dexamethasone Cream group are compared with model group, * P <
0.05, * * P < 0.01, * * * P < 0.001.
Attached drawing 7 is silk polymerization gene deletion mouse each group dermatitis appraisal result statistical chart, and note: Variant statistical meaning is with *
It indicates, * P < 0.05, * * P < 0.01, * * * P < 0.001.
Attached drawing 8 is silk polymerization gene deletion mouse each group scratching frequency result statistical chart, and note: Variant statistical meaning is with *
It indicates, * P < 0.05, * * P < 0.01, * * * P < 0.001.
Attached drawing 9 is relative expression's result statistical chart of the skin lesion mRNAIL-4 of silk polymerization gene deletion mouse each group mouse,
Note: model group ###P < 0.001 compared with normal group, compared with model group, NS is for each concentration C K group and Dexamethasone Cream group
No significant difference, * P < 0.05, * * P < 0.01, * * * P < 0.001.
Specific embodiment
The invention will be further elucidated with reference to specific embodiments.It should be understood that these embodiments are merely to illustrate this hair
It is bright rather than limit the scope of the invention.In addition, it should also be understood that, after having read the content of the invention recorded, art technology
Personnel can make various changes or modifications the present invention, and such equivalent forms equally fall within the application the appended claims and limited
Fixed range.
In following examples, related percentage is calculated in weight percent, institute's employment unless otherwise indicated
Ginseng saponin(e CK (purity > 98.0%) is purchased from Sichuan Wei Keqi Biotechnology Co., Ltd.
The drug constitutive material and weight percent content of embodiment 1-10 is as shown in table 1.
Table 1
Embodiment 1-5 treats atopic dermatitis externally-applied soft ointment
Ginsenoside compound K and conventional pharmaceutical carrier are taken according to constituent weight percent content in table 1 respectively, according to ointment
The preparation of agent conventional preparation method, it is sealed, it is spare.
Embodiment 6-10 treats atopic dermatitis makeup healthcare mist spray
Ginsenoside compound K and conventional pharmaceutical carrier are taken according to constituent weight percent content in table 1 respectively, according to makeup
The preparation of healthcare mist spray conventional preparation method, it is sealed, it is spare.
11 zoopery of embodiment (one)
This experiment is by establishing the atopic dermatitis mouse model of the percutaneous sensitization induction of ovalbumin antigen (OVA) and dividing
Group observes each group then respectively with Ginsenoside compound K (basic, normal, high concentration), positive drug (dexamethasone) to mouse topical administration
Curative effect after mouse medication.
One, experimental material
1, experimental animal:
Balb/c mouse (female, 6 week old, SPF grades, quantity 60), raises in animal house, animal house is maintained
The period of 12:12 hours Light-Darks, temperature are 25 ± 2 DEG C and humidity 55 ± 15%.With standard laboratory diet
(LabDiet autoclave sterilization rodent diet (LabDietAutoclavableRodentDiet5010), PMI international camp
Support, Brentwood, USA) feeding mouse, it adapts to after two weeks, carry out OVA sensitization.
2, OVA is bought from Sigma-Aldrich (St.Louise, MO),
Ginsenoside compound K (purity > 98.0%) is purchased from Sichuan Wei Keqi Biotechnology Co., Ltd.
Two, experimental method
1, the foundation of AD model
Divide 60 female Balb/c mouse to cage at random, 10, every cage, all experimental implementations meet having for animal welfare
Close regulation.
Skin is pasted with adhesive fabric after all back of mice shavings, leads to horny layer of epidermis slight damage.OVA antigen is molten
Drop is fixed after on 1 × 1 square centimeter of sterile gauze, being affixed on skin with Tegaderm adhesive tape, and continuous 1 week, be the
Primary percutaneous sensitization (the 1-7 days).Interval 2 weeks and then it is secondary with identical method adhesive fabric stickup skin after, antigen is set
In skin 1 week, implement second of percutaneous sensitization (the 21-28 days).After 2 weeks in the same way, third and fourth percutaneous cause is carried out
Quick (the 42-49 days, the 63-70 days) 10 weeks in total, observe weekly mouse skin lesion situation, and with the 36th day from be administered continuously it is outer
In the 71st day collecting sample after applying 5 weeks.AD model foundation process is as shown in Figure 1.
2, grouping and administration
60 mouse are divided into solvent control group (NC), model group (MC), low concentration CK group according to random digits table
(LD), middle concentration C K group (MD), high concentration CK group (HD), dexamethasone in treatment group (DXM), it is every group 10, percutaneous in third time
While sensitization, using relative medicine external curing 35 days (the 36-70 days), each group mouse situation is observed and recorded.
It is 4%, HD group Drug level is 8% that the LD group concentration, which is 2%, MD group Drug level, density calculating method are as follows:
Concentration=Ginsenoside compound K quality/solvent quality.
3, result recording method
The AD mouse dermatitis of 3.1OVA sensitization is scored
The skin lesion at the 7th day (the 2nd time point), the 28th day (the 3rd time point), the 70th day (the 4th time point) after OVA excitation
Severity determines that standards of grading are as follows, and two experimenters are to model group and treatment group mouse by dermatitis reaction standards of grading
Skin lesion, in terms of following four (erythema, oedema, exudation, drying/scratch), score value indicates severity: 0 (nothing), and 1 is (light
Degree), 2 (moderates) and 3 (severes) score, and scoring summation result takes mean.
The AD mouse of 3.2OVA sensitization scratches number
It observes AD mouse and scratches phenomenon, scratching back lesions position skin calculates 1 effectively scratching, and the continuous 3s or more that scratches is pressed
2 calculating, and manual intervention makes mouse stop this scratching behavior after 3s, counts 5min mouse and scratches number.
The atopic dermatitis model mouse skin lesion pathologic condition record of 3.3OVA sensitization induction
Mouse skin tissue after taking experiment, is HE and dyes and analyze epidermis and dermis thickness.
Three, experimental result
1, the AD mouse fash severity score result of OVA sensitization
Mouse dermatitis appraisal result as shown in Fig. 2, model group mouse dermatitis scoring increase with the extension of sensitization time,
Each group mouse dermatitis diversity of values is not statistically significant, shows modeling success.The mouse of LD, MD, HD group and DXM group is through treating
Afterwards, dermatitis scoring is declined, and difference is statistically significant (P < 0.05).Dermatitis after LD group and the treatment of DXM group mouse
Diversity of values is not statistically significant.And MD group and HD the group difference compared with DXM group have statistical significance.The above experimental result table
Bright, Ginsenoside compound K can reduce the AD model mice dermatitis scoring of OVA sensitization, and middle concentration group and high concentration group curative effect are higher than low dense
Degree group and Dexamethasone Cream group.
2, the AD mouse of OVA sensitization scratches appraisal result
Mouse scratches appraisal result as shown in figure 3, the scratching frequency of model group mouse increases with the extension of sensitization time,
Each group mouse scratches frequency no significant difference before the treatment.The mouse of LD, MD, HD group and DXM group is after treating, scratching
The frequency is reduced, and difference is statistically significant (P < 0.05).Scratching frequency drop after LD group and the treatment of DXM group mouse
Low no significant difference.And MD group and HD the group difference compared with DXM group have statistical significance (P < 0.05).More than
The experimental results showed that Ginsenoside compound K can reduce the AD model mice scratching frequency of OVA sensitization, middle concentration group and high concentration group are treated
Effect is higher than low dose group and Dexamethasone Cream group.
3, the atopic dermatitis model mouse skin lesion pathologic condition result of OVA sensitization induction
Experimental result is as shown in Figure 4-Figure 6, and mouse skin lesion pathological examination is shown, the significant hyperplasia of epidermis is formed with ulcer；
Corium acanthosis, with the infiltration of inflammatory cell.After each concentration Ginsenoside compound K external application, epidermis and dermis thickness and model
Group is compared and is reduced, and difference has statistical significance.Data show that the Ginsenoside compound K therapeutic effect of middle concentration is most
It is good, it is good for the inhibiting effect of epidermis and corium hyperplasia.
Four, experiment conclusion
It is above-mentioned the results showed that Ginsenoside compound K has therapeutic effect to the atopic dermatitis mouse of OVA sensitization, in it is dense
Degree group improves the most significant.
12 zoopery of embodiment (two)
This experiment, which is polymerize by choosing silk, gene deletion mouse model and to be grouped, then respectively with Ginsenoside compound K (it is low,
Middle and high concentration), positive drug (dexamethasone) to mouse topical administration, observe curative effect after the medication of each group mouse.
One, experimental material
1, experimental animal
Silk polymerization gene deletion mouse (FlakyTail, ft) is a kind of spontaneity AD model mice, and 32 week old can be in face
And there is apparent ulceration, exudation and dry furfur and is consistent with itch with clinical AD patient symptom in neck.Silk polymerization gene
Mouse is purchased from U.S. Jackson company (Jackson, USA), through close breeding method group expanding born of the same parents, chooses the Ft of 50 32 week old
Mouse.
10 C57BL6/J mouse.
2, Ginsenoside compound K (purity > 98.0%) is purchased from Sichuan Wei Keqi Biotechnology Co., Ltd.
Two, experimental method
Mice group and administration
Ft mouse is divided into five groups according to the scoring of its dermatitis: model group, CK low concentration group (LD), concentration group (MD) in CK,
CK high concentration group (HD), Dexamethasone Cream group (DXM).10 C57BL6/J mouse are as Normal group.Due to mouse skin
Damage mostly occurs in Face and cheek and neck, therefore will be applied to herein outside drug, continuous observation mouse dermatitis scoring after smearing for four weeks
With the change of IL-4 expression at scratching number improvement situation and skin lesion, mouse dermatitis scores and scratches number evaluation criterion and this paper
The evaluation criterion of middle OVA sensitized mice is consistent, and (score value indicates severity: 0 (nothing), 1 (slight), 2 (moderates) and 3 (severes)
Score, scoring summation result takes mean), the mRNA relative expression quantity of Th2 cytokines IL-4 is by RT-PCR at skin lesion
Method detection.
It is 4%, HD group Drug level is 8% that the LD group concentration, which is 2%, MD group Drug level, density calculating method are as follows:
Concentration=Ginsenoside compound K quality/solvent quality.
Three, experimental result
1, the scoring of each group silk polymerization gene deletion mouse dermatitis and scratching frequency experimental result
As a result as shown in Fig. 7-Fig. 8, after treating, dermatitis is scored and is scratched the CK group mouse of each concentration (basic, normal, high concentration)
It grabs number to be declined, and difference is statistically significant.Dermatitis is commented after low concentration CK group is treated with high concentration CK group mouse
Divide no significant difference.And middle concentration group difference compared with low concentration group has statistical significance.Middle concentration C K group mouse
Scratching number declines the most significant compared with other concentration Cs K group.The pretherapy and post-treatment dermatitis of Dexamethasone Cream group mouse is scored and is scratched
Grab number no significant difference.The experimental results showed that, Ginsenoside compound K can reduce the scoring of Ft mouse dermatitis and scratching above
The frequency, middle concentration group curative effect are higher than low concentration group and high concentration group, and Dexamethasone Cream causes skin for silk polymerization gene deletion
The atopic dermatitis sample skin lesion of skin barrier function exception does not have improvement result.
2, relative expression's result of each group silk polymerization gene deletion mouse skin lesion mRNAIL-4
Experimental result is as shown in figure 9, model group IL-4 compared with Normal group is significantly expressed and difference has statistics
Meaning；The IL-4 expression compared with model group of the CK group of each concentration is declined, and difference is statistically significant, wherein in it is dense
CK group is spent compared with other concentration groups, and the expression decline of IL-4 is the most obvious.Dexamethasone Cream group is compared with model group, skin lesion
The differential expression for locating IL-4 is not statistically significant.Experimental data shows that CK external application has the expression of IL-4 at Ft mouse skin lesion
Reduced effect, middle concentration C K group improvement highly expressed for mouse IL-4 is best, and dexamethasone is for Ft mouse skin
The reduction that IL-4 is expressed at damage influences smaller.
Four, experiment conclusion
The above experimental data shows that Ft mouse has the mutation of silk polymerization gene, the expression of silk polymeric protein in skin
Inhibit, barrier function is destroyed, and is stimulated vulnerable to external antigen, and the skin lesion of atopic dermatitis sample is formed.Ginsenoside compound K can improve
Skin lesion form and the expression for reducing Th2 cytokines IL-4 at skin lesion, middle concentration group curative effect are more significant.And ground plug rice
Pine does not have therapeutic effect to Ft mouse.It may be to aggravate barrier since hormone can cause a polyprotein synthesis to further suppress
Damage.And Ginsenoside compound K does not have silk polyprotein to synthesize inhibiting effect, more there is the possibility for repairing barrier, exotic antigen percutaneous absorbtion
After reduction, skin lesion is improved.
The present invention respectively gives mouse by establishing the atopic dermatitis mouse model of OVA sensitization, choosing Ft mouse
Medicine: using the Ginsenoside compound K and positive drug (Dexamethasone Cream) of basic, normal, high concentration, experiment conclusion is obtained: (1) ginseng soap
Glycosides CK has therapeutic effect to the atopic dermatitis mouse of OVA sensitization, and middle concentration group improvement is the most significant, and curative effect and hormone phase
When；(2) Ginsenoside compound K can improve Ft mouse skin lesion form and reduce the expression of Th2 cytokines IL-4 at skin lesion,
Middle concentration group curative effect is more significant.And dexamethasone does not have therapeutic effect to Ft mouse.Therefore, Ginsenoside compound K can be used for making
Standby treatment atopic dermatitis external drug and makeup health care product.
The present invention indicates that Ginsenoside compound K is used to prepare the drug and makeup health care product for the treatment of atopic dermatitis for the first time, with
Drug used in the prior art compares, Ginsenoside compound K good, few side effects, recurrence with curative effect when treating atopic dermatitis
Low, the safer advantage of rate.
The above is only a preferred embodiment of the present invention, it is noted that for the ordinary skill people of the art
Member, without departing from the principle of the present invention, can also make several improvement and supplement, these are improved and supplement also should be regarded as
Protection scope of the present invention.
Claims (9)
1. application of the Ginsenoside compound K in preparation treatment atopic dermatitis external drug.
2. applying according to claim 1, which is characterized in that the Ginsenoside compound K is in treatment atopic dermatitis external drug
In shared parts by weight percentage be 0.1-99.9%.
3. applying according to claim 1, which is characterized in that the treatment atopic dermatitis external drug is by ginsenoside
The excipient or carrier that CK and external drug allow are made.
4. applying according to claim 1, which is characterized in that the dosage form packet of the treatment atopic dermatitis external drug
Include ointment, cream, liniment, spray and film.
5. application of the Ginsenoside compound K in the makeup health care product of preparation treatment atopic dermatitis.
6. applying according to claim 5, which is characterized in that the Ginsenoside compound K is in treatment atopic dermatitis makeup health care
Shared parts by weight percentage is 0.1-99.9% in product.
7. applying according to claim 5, which is characterized in that the treatment atopic dermatitis makeup health care product is by ginseng soap
The excipient or carrier that glycosides CK and makeup health care product allow are made.
8. -7 any application according to claim 1, which is characterized in that the atopic dermatitis includes simple form and mixing
Type.
9. -7 any application according to claim 1, which is characterized in that the atopic dermatitis includes that at least one is selected from such as
Under symptom: (1) pruritus；(2) rubescent and bleeding；(3) edema；(4) damage and tissue damage；(5) crust and drying are formed.
Priority Applications (1)
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Cited By (6)
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| CN111281908A (en) * | 2020-04-10 | 2020-06-16 | 青蛙王子（福建）婴童护理用品有限公司 | Anti-eczema traditional Chinese medicine extract and preparation method and application thereof |
| CN111903605A (en) * | 2020-07-27 | 2020-11-10 | 广州市皮肤病防治所(广州市性病防治监测中心) | Induced SD rat hormone-dependent dermatitis model and determination method thereof |
| CN112843113A (en) * | 2021-03-23 | 2021-05-28 | 南京医科大学 | A preparation for treating contact dermatitis |
| CN113892461A (en) * | 2021-10-28 | 2022-01-07 | 中国农业大学 | Construction method of wheat gluten protein transdermal sensitization mouse model |
| CN117899098A (en) * | 2024-03-19 | 2024-04-19 | 昆明之诺医药科技有限公司 | Application of rare ginsenoside CMx in preparation of medicine for preventing and/or treating type 2 inflammatory diseases |
| CN117899098B (en) * | 2024-03-19 | 2024-05-17 | 昆明之诺医药科技有限公司 | Application of rare ginsenoside CMx in preparation of medicine for preventing and/or treating type 2 inflammatory diseases |
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| Publication number | Priority date | Publication date | Assignee | Title |
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| CN111281908A (en) * | 2020-04-10 | 2020-06-16 | 青蛙王子（福建）婴童护理用品有限公司 | Anti-eczema traditional Chinese medicine extract and preparation method and application thereof |
| CN111903605A (en) * | 2020-07-27 | 2020-11-10 | 广州市皮肤病防治所(广州市性病防治监测中心) | Induced SD rat hormone-dependent dermatitis model and determination method thereof |
| CN112843113A (en) * | 2021-03-23 | 2021-05-28 | 南京医科大学 | A preparation for treating contact dermatitis |
| CN112843113B (en) * | 2021-03-23 | 2022-02-01 | 南京医科大学 | A preparation for treating contact dermatitis |
| CN113892461A (en) * | 2021-10-28 | 2022-01-07 | 中国农业大学 | Construction method of wheat gluten protein transdermal sensitization mouse model |
| CN117899098A (en) * | 2024-03-19 | 2024-04-19 | 昆明之诺医药科技有限公司 | Application of rare ginsenoside CMx in preparation of medicine for preventing and/or treating type 2 inflammatory diseases |
| CN117899098B (en) * | 2024-03-19 | 2024-05-17 | 昆明之诺医药科技有限公司 | Application of rare ginsenoside CMx in preparation of medicine for preventing and/or treating type 2 inflammatory diseases |
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