CN118286223A - Use of AT-007 in preventing and treating androgenetic alopecia - Google Patents
Use of AT-007 in preventing and treating androgenetic alopecia Download PDFInfo
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Abstract
The invention relates to the technical field of medicines, and discloses application of AT-007 in preventing and treating androgenetic alopecia. In order to solve the technical problem of preventing and treating androgenetic alopecia, the invention applies AT-007 to intervening in DHT-induced AGA model mice, which shows that AT-007 has the effects of promoting hair regeneration, increasing hair length and hair follicle melanin generation, and can effectively resist hair loss caused by DHT. Based on the above, a new scheme for treating androgenetic alopecia is provided for preventing and/or treating androgenetic alopecia.
Description
Technical Field
The invention relates to the technical field of medicines, in particular to application of AT-007 in preventing and treating androgenetic alopecia.
Background
Androgenetic alopecia (Androgenetic Alopecia, AGA), also known as seborrheic alopecia or premature alopecia, is a common alopecia disorder characterized by hair follicle miniaturization and progressive hair loss, the most common type of male pattern baldness, but can also occur in females. AGA is gradually converted to vellus hair by genetic susceptibility and androgen-hypersensitive hair follicles to scalp terminal hair, with high prevalence and possibly severe psychological and social effects. The pathogenesis of AGA is closely related to the biological effects of androgens. Androgens are important hormones in the growth and development of the human body, testosterone is the main and most active androgen in men, and testosterone is converted into dihydrotestosterone (dihydrotestosterone, DHT) by type II 5-a reductase (SRD 5 A2). Androgen Receptor (AR) in hair follicle has a strong affinity for DHT compared to testosterone, and when excessive DHT is present, AR binds to DHT, changes the protein shape, and initiates a signaling cascade to miniaturize hair follicle, thereby affecting the normal growth cycle of hair.
Currently, treatment of AGA still faces a number of challenges. The U.S. food and drug administration has only approved two drugs for AGA treatment: minoxidil and oral finasteride are topically applied. Minoxidil is capable of promoting blood circulation of hair follicles, thereby stimulating hair growth, but its therapeutic effect is often temporary. Finasteride, as a competitive and specific 5 alpha-reductase inhibitor, is effective in reducing DHT production, slowing or reversing the hair loss process, but finasteride application may be accompanied by side effects such as sexual dysfunction. In addition to the above drugs, there are several emerging therapeutic technologies currently being used in the treatment of AGA, including microneedle therapy, platelet rich plasma injection, low intensity laser therapy, hair follicle transplantation surgery, and the use of adipose tissue-derived stem cell component extracts. While these methods provide more treatment options for AGA patients, there are individual limitations. For example, these treatments vary greatly in effect from individual to individual, the cost of treatment can be very high, and the safety and long-term efficacy of certain techniques have not been fully investigated and validated. Thus, there is a need to develop more safe and effective treatment regimens.
Healthy and beautiful hair can give people a good image, so that people can feel more confident in interpersonal interaction, and people pay more attention to preventing and treating alopecia. In the field, a safe and efficient medicine is still needed to be searched for effectively preventing and treating androgenetic alopecia.
Disclosure of Invention
In order to solve the technical problem of preventing and treating androgenetic alopecia, the invention provides application of AT-007 in preventing and treating androgenetic alopecia. The invention researchers apply AT-007 to intervening in DHT-induced AGA model mice, which shows that AT-007 has the effects of promoting hair regeneration, increasing hair length and hair follicle melanogenesis, and can effectively resist hair loss caused by DHT. Based on the above, a new scheme for treating androgenetic alopecia is provided for preventing and/or treating androgenetic alopecia.
The specific technical scheme of the invention is as follows:
in a first aspect, the present invention provides the use of AT-007 for the preparation of a product for the prevention and/or treatment of androgenetic alopecia.
In the study of AGA patients, researchers of the present invention found that the expression of sorbitol dehydrogenase (SORD) was decreased at the skin lesions of AGA patients compared to those at non-skin lesions. And experiments prove that the phenomenon can be related to the progress of AGA. Based on this result, the inventors further used AT-007 to intervene in DHT-induced AGA model mice to determine the effect of AT-007 on hair loss during AGA progression, and expected to provide a new regimen for treatment of AGA.
AT-007 is an aldose reductase inhibitor and is currently used primarily in the treatment of the rare childhood metabolic disease galactosylemia. The invention is applied to intervening the AGA model mice induced by DHT by researchers, which shows that AT-007 has the effects of promoting hair regeneration, increasing hair length and generating hair follicle melanin, and can effectively resist hair loss caused by DHT. Based on this, a new method for preventing and/or treating androgenetic alopecia can be provided.
Preferably, the product is a medicine, a daily chemical product, a food or a food additive.
As a preference of the above-described solution of the invention, the product intervenes and/or treats androgenic alopecia by counteracting DHT-induced inhibition of hair follicle growth. The product is preferably a pharmaceutical, daily chemical, food, or food additive that resists inhibition of hair follicle growth by DHT.
The application of AT-007 in relieving the hair loss of mice under the stimulation of DHT and the related molecular mechanism are discussed, so that the effectiveness of AT-007 in inhibiting the abnormal growth of hair follicles of mice caused by dihydrotestosterone is clear, the feasibility of AT-007 in promoting hair regeneration is also proved, the basis is provided for intervention or treatment of androgenetic alopecia, and the feasibility of AT-007 in intervention and/or treatment of androgenetic alopecia by resisting the inhibition of hair follicle growth caused by DHT is provided.
In a second aspect, the present invention provides an article of manufacture for treating androgenetic alopecia, the active ingredient of the article comprising AT-007.
The invention researchers apply AT-007 to intervening in DHT-induced AGA model mice, which shows that AT-007 has the effects of promoting hair regeneration, increasing hair length and hair follicle melanogenesis, and can effectively resist hair loss caused by DHT. Based on this, an article for treating androgenetic alopecia can be provided for preventing and/or treating androgenetic alopecia, the active ingredient of which comprises AT-007.
As a preferred embodiment of the present invention, the active ingredient of the product is AT-007.
Preferably, the product is a pharmaceutical product, a daily chemical product, a food product, or a food additive.
As a preference of the above-described solution of the invention, the preparation intervenes and/or treats androgenic alopecia by counteracting DHT-induced inhibition of hair follicle growth. The article is preferably a pharmaceutical, daily chemical, food, or food additive that resists inhibition of hair follicle growth by DHT.
The application of AT-007 in relieving the hair loss of mice under the stimulation of DHT and the related molecular mechanism are discussed, so that the effectiveness of AT-007 in inhibiting the abnormal growth of hair follicles of mice caused by dihydrotestosterone is clear, the feasibility of AT-007 in promoting hair regeneration is also proved, the basis is provided for intervention or treatment of androgenetic alopecia, and the feasibility of AT-007 in intervention and/or treatment of androgenetic alopecia by resisting the inhibition of hair follicle growth caused by DHT is provided.
Compared with the prior art, the invention has the following technical effects:
The invention researchers apply AT-007 to intervening in DHT-induced AGA model mice, which shows that AT-007 has the effects of promoting hair regeneration, increasing hair length and hair follicle melanogenesis, and can effectively resist hair loss caused by DHT. Based on the above, a new scheme for treating androgenetic alopecia is provided for preventing and/or treating androgenetic alopecia.
Drawings
FIG. 1 is a graph showing the hair growth of mice in example 1 of the present invention at various times;
FIG. 2 is a graph showing H & E staining of the back skin of each group of mice after 28 days of treatment in example 2 of the present invention;
FIG. 3 is a graph showing the results of melanin staining of the skin of each group of mice in example 3 of the present invention.
Detailed Description
The invention is further described below with reference to examples. Those of ordinary skill in the art will be able to implement the invention based on these descriptions. In addition, the embodiments of the present invention referred to in the following description are typically only some, but not all, embodiments of the present invention. Therefore, all other embodiments, which can be made by one of ordinary skill in the art without undue burden, are intended to be within the scope of the present invention, based on the embodiments of the present invention.
The experimental animals used in the embodiment of the invention are: 15 male C57BL/6 mice (50 g.+ -. 0.2 g) were purchased at the Hangzhou medical laboratory animal center for 6 weeks of age, and all were kept under this center clean grade.
In the embodiment of the invention, the hematoxylin eosin staining kit is purchased from Shanghai Biyun biotechnology limited company; dihydrotestosterone (mildrolone), available from Shanghai microphone Biochemical technologies Co., ltd; AT-007, CAS number 2170729-29-8, available from TargetMol; dimethyl sulfoxide (DMSO), available from Sigma-Aldrich; melanin-staining fluid (ferrous sulfate process), available from the pearl oyster Caddy Biotechnology Co.
EXAMPLE 1 establishment and administration of AGA mouse model
(1) Preparation of experiments
Newly purchased male C57BL/6 mice were subjected to 7 days of adaptive rearing before the start of the experiment. Subsequently, the mice were randomly divided into three experimental groups of 5 mice each according to the random principle. The three experimental groups were:
control group: only shaving operations were performed without any treatment.
DHT group: DHT was subcutaneously injected to induce the AGA model.
AT-007/DHT group: DHT was subcutaneously injected with the aid of AT-007 treatment (AT-007 intraperitoneal injection).
(2) Modeling and administration
Day 0: on the first day of the experiment, all mice were shaved on their backs and applied with depilatory cream, with the criteria of 2 square centimeters (2 cm. Times.2 cm) of hair removal.
Day 1 to Day28: starting on the first Day of the experiment (Day 1), mice of the DHT group and AT-007/DHT group received a 200 μl subcutaneous injection of DHT solution once daily for 28 consecutive days. AT the same time, the AT-007/DHT group mice received an additional daily intraperitoneal injection of the same dose of AT-007 solution.
(3) Observing and recording shooting records: on days 0, 8, 15, 21 and 28 of the experiment, the back treated area of the mice was photographed to record the growth of hair, as shown in fig. 1. In FIG. 1, control represents a Control group, DHT represents a DHT group, and AT-007/DHT represents an AT-007/DHT group.
Day 28: at the end of the experiment, back skin samples of all mice were collected for biological index analysis of example 2 and example 3.
Example 2 hematoxylin-eosin (H & E) staining of mouse skin tissue
A skin sample of 1 square centimeter (1 cm. Times.1 cm) was taken from the back of the mice, fixed with 4% paraformaldehyde, dehydrated and paraffin embedded, and 5 μm slices were cut and baked in an oven at 60 ℃. Then treated in xylene for 15min to remove paraffin, followed by a second soak to ensure adequate dewaxing. Next, the sections were stained in an aqueous hematoxylin solution for 5min, followed by washing with running water for 15min. After staining, the sections were dehydrated step by step in 75% and 90% ethanol for 10min per stage. Finally, the sections were immersed in 0.5% ethanol-eosin staining solution for 2min and rinsed with running water for 1min. The dyed slice is dehydrated by absolute ethyl alcohol and then is transparent treated in dimethylbenzene again for 3min, and the process is repeated once. Thereafter, the encapsulation was performed using a neutral resin. The sections after the sealing were placed under a microscope for observation and photographing.
The H & E staining results of the back skin of each group of mice after 28 days of treatment are shown in fig. 2, including H & E staining observation (a), hair follicle length statistics (b) and skin thickness statistics (c). In FIG. 2, control represents a Control group, DHT represents a DHT group, and AT-007/DHT represents an AT-007/DHT group.
Example 3 preparation of skin melanin-stained sections of mice: the sections of example 2 were placed in a 55℃incubator for 30min pre-heating to complete dewaxing and antigen retrieval. Cleaning: the sections were washed 1 time with distilled water. Melanin staining: the sections were treated with ferrous sulfate solution for 1 hour. Cleaning: the solution was again washed 3 times with distilled water. The reaction: dropwise adding potassium ferricyanide acetic acid solution, and treating for 30min. Cleaning: washing with glacial acetic acid solution for 3s and spin-drying. Van Gieson dyeing: dyeing for 1min. Dehydration and transparency: the mixture is treated with 95% ethanol for 30s, dehydrated with absolute ethanol and finally subjected to transparent treatment with xylene. Sealing piece: the encapsulation was performed with neutral gum.
The melanin-staining results of the skin of each group of mice were observed and photographed and subjected to quantitative analysis of melanin staining by the following method: and (3) using IHC Toolbox of Image J software to frame and select the color of the positive part, then automatically sketching the positive area of the melanin dyeing, adjusting a proper color threshold, respectively selecting the positive area and all the dyeing areas to obtain an area value, and calculating the percentage of the positive area/the total area of the melanin dyeing to obtain a result.
The results of melanin staining of the skin of each group of mice are shown in FIG. 3. In FIG. 3, control represents a Control group, DHT represents a DHT group, and AT-007/DHT represents an AT-007/DHT group.
Data analysis
① Figure 1 shows back hair growth of control, DHT and AT-007/DHT mice on days 0, 8, 15, 21 and 28 of the experiment. On days 8 and 15 of the early trial, mice in the control group and the AT-007/DHT group showed significant hair regrowth, while the back skin of the DHT group mice remained pink with no hair growth. As the experiment proceeded to day 21 and day 28, the control group had hair restoration near complete regeneration, and the AT-007/DHT group mice had more pronounced hair regeneration and darkened skin color. In contrast, DHT group mice did not begin to exhibit local hair regrowth until day 28 of the experiment.
The results indicate that AT-007 can promote hair regeneration in DHT-induced AGA model mice.
② Fig. 2 shows the H & E staining results for each treatment group. The staining results of figures 2a and 2b show that anagen hair was longer in the AT-007/DHT group than in the DHT group mice and the differences were statistically significant (P < 0.0001), AT-007/DHT group hair was longer than in the Control group and the differences were statistically significant (p=0.0055). Comparison of the dermis thickness results for each treatment group (FIGS. 2a and 2 c) shows that both the Control and AT-007/DHT groups have dermis thicknesses thicker than that of the DHT group and that the difference is statistically significant (P < 0.05), but the difference in dermis thickness for the Control and AT-007/DHT groups is not statistically significant. AT-007 was shown to interfere with DHT-induced hair growth inhibition and dermal thickness thinning with hair regrowth promoting effects.
③ Fig. 3 uses ferrous sulfate to evaluate melanin levels in the skin of different groups of mice. As can be seen from FIG. 3, the skin of the mice in the DHT group had little melanin staining, the Control group and the AT-007/DHT group had higher levels of melanin than the DHT group and the difference was statistically significant (P < 0.05), but the difference between the Control group and the AT-007/DHT group was not statistically significant. It was shown that AT-007 may promote melanogenesis.
Therefore, based on the above results, it was revealed that AT-007 has the effects of promoting hair regeneration, increasing hair length and melanogenesis of hair follicle. Can effectively resist hair loss caused by DHT, shows the potential value of AT-007 in treating AGA, and provides a new scheme for AGA treatment.
The raw materials and equipment used in the invention are common raw materials and equipment in the field unless specified otherwise; the methods used in the present invention are conventional in the art unless otherwise specified.
The foregoing description is only a preferred embodiment of the present invention, and is not intended to limit the present invention, and any simple modification, variation and equivalent transformation of the above embodiment according to the technical substance of the present invention still fall within the scope of the technical solution of the present invention.
Claims (7)
- Use of at-007 for the preparation of a product for the prevention and/or treatment of androgenetic alopecia.
- 2. The use according to claim 1, wherein: the product is a medicine, daily chemical product, food or food additive.
- 3. The use according to claim 2, wherein: the product is a drug, daily chemical product, food, or food additive for resisting hair follicle growth inhibition caused by DHT.
- 4. An article of manufacture for treating androgenetic alopecia, characterized in that: the active ingredient of the article comprises AT-007.
- 5. The article of claim 4 for treating androgenetic alopecia, wherein: the active ingredient of the product is AT-007.
- 6. The article of claim 4 for treating androgenetic alopecia, wherein: the product is a medicine, daily chemical product, food or food additive.
- 7. The article of manufacture for treating androgenetic alopecia of claim 6, wherein: the product is a drug, daily chemical product, food, or food additive for resisting hair follicle growth inhibition caused by DHT.
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