CN116392505A - Use of molybdenum nanoparticles in the preparation of a medicament for the treatment of hair growth - Google Patents

Abstract

The present invention provides the use of molybdenum nanoparticles in the preparation of medicines for treating hair growth. The invention also provides a pharmaceutical composition for treating hair growth, which is composed of molybdenum nano particles and minoxidil. The present invention also provides the use of the combination of molybdenum nanoparticles and minoxidil in the preparation of medicine for treating hair growth. The molybdenum nanoparticles selected in the present invention may promote hair growth by down-regulating ROS, and nanoscale molybdenum can accelerate hair growth, increase the number of local hair follicles, and reduce the expression of molecules related to oxidative stress, such as iNOS, COX ₂ , and androgen receptor. Research has shown that nanoscale molybdenum is a potential topical drug for the treatment of hair loss by inhibiting oxidative stress pathways.

Description

Use of molybdenum nanoparticles in the preparation of medicines for treating hair growth

technical field

The invention belongs to the field of biomedicine and relates to a hair growth drug, in particular to the use of molybdenum nanoparticles in the preparation of a drug for treating hair growth.

Background technique

Alopecia is a multifactorial disease prevalent among millions of people worldwide, characterized by hair loss, including various types such as alopecia areata, androgenetic alopecia, and others. For example, androgenetic alopecia (AGA) affects more than 50% of the population in terms of population proportion alone, with a major negative impact on the patient's quality of life. Topical minoxidil is one of the Food and Drug Administration (FDA)-approved treatments for different types of hair loss, ranging from AGA to alopecia areata (AA). However, minoxidil has limitations in the treatment of hair loss, such as slow action, low efficacy, and inability to effectively inhibit excessive oxidative stress, a major etiological factor of hair loss. Clinical responses to minoxidil usually take 3-6 months to be observed, and efficacy in the overall population remains relatively low at 30-40%. Shortening the reaction time and increasing the curative effect can relieve the psychological burden of hair loss patients. Hair growth is closely related to the clinical response of patients with alopecia, so treatments that can accelerate hair growth may be a solution to address hair loss.

Oxidative stress has been identified as a pathway closely related to hair growth. Substances that can reduce oxidative stress have the potential to promote hair growth. A key step in down-regulating oxidative stress is the reduction of reactive oxygen species (ROS). Therefore, substances with rapid response to scavenge ROS may be the key to potential treatments. Metal nanoparticles have been widely documented as antioxidants ranging from 1 to 100 nm due to their ability to inhibit the generation of oxidative radicals either through the chain scission process or through the chelation process. Among these nanoparticles, molybdenum, one of the essential metallic elements in the human body, showed potential to fight oxidative stress, even without the nanoscale appearance. For example, molybdenum-containing nanomaterials show POD-like activity to efficiently catalyze the decomposition of _H2O2 to generate _˙OH , which is essential for reducing ROS.

Contents of the invention

In view of the above technical problems in the prior art, the present invention provides the use of molybdenum nanoparticles in the preparation of medicines for treating hair growth, and the use of the molybdenum nanoparticles in the preparation of medicines for treating hair growth is to The technical problem that the effect of the medicine in the prior art is not good for the treatment of alopecia.

The invention provides the use of molybdenum nano particles in the preparation of medicine for treating hair growth.

Further, the molybdenum nanoparticles are nanoscale molybdenum monomers.

Specifically, molybdenum nanoparticles are dissolved in physiological saline for use.

The invention also provides a pharmaceutical composition for treating hair growth, which is composed of molybdenum nano particles and minoxidil.

Concrete, by the physiological saline solution of molybdenum nanoparticle and minoxidil organic solution according to volume ratio 1:1 composition, the concentration of the physiological saline solution of described platinum nanoparticle is 33ppm, the mass volume of minoxidil organic solution The ratio is 5g/100Ml.

The present invention also provides the use of the combination of molybdenum nanoparticles and minoxidil in the preparation of medicine for treating hair growth.

Oxidative stress has been identified as one of the underlying mechanisms of hair loss because it can cause damage to the hair follicle and disrupt hair growth. Transition metal elements with fast electron transfer, such as molybdenum, have been widely studied and applied to suppress oxidative stress. Molybdenum, one of the essential trace elements in the human body, has the potential to inhibit oxidative stress. Due to its physicochemical properties, nanoscale molybdenum can mediate oxidative stress more quickly.

Our results showing that molybdenum alone was able to accelerate hair growth in mice were confirmed by representative photographs under a skin microscope and hair density analysis. Hair length in the molybdenum group was comparable to that in the minoxidil group. Furthermore, the combination of molybdenum and minoxidil showed a more pronounced hair growth effect than minoxidil alone. The number of hair follicles was upregulated in the molybdenum group compared with the NaCl group. Furthermore, there was no significant difference between the molybdenum and minoxidil groups in terms of hair follicle number, suggesting that molybdenum may be a viable alternative topical treatment for hair loss in addition to minoxidil.

Oxidative stress can lead to hair follicle damage, which is an important factor associated with hair loss. Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are enzymes involved in inflammatory responses, and their expression is associated with hair follicle oxidative stress. iNOS is an enzyme that catalyzes the production of nitric oxide (NO), a free radical that promotes oxidative stress and hair loss. In hair follicles, iNOS is expressed in the outer root sheath and dermal papilla cells. Under conditions of oxidative stress, such as exposure to UV radiation, increased expression of iNOS was observed in hair follicles. This increased expression of iNOS can lead to increased NO production, which leads to oxidative damage to the hair follicle and subsequent hair loss. COX-2 is an enzyme involved in the synthesis of prostaglandins, lipid mediators that regulate inflammation and immune responses. In hair follicles, COX-2 is expressed in the outer root sheath, dermal papilla cells, and sebaceous glands. Under oxidative stress conditions, the expression of COX-2 is increased in hair follicles, and its activity can promote ROS production and oxidative damage. In addition, prostaglandins produced by COX-2 can stimulate the expression of iNOS, further aggravating oxidative stress and hair loss. Our data suggest that both iNOS and COX-2 may be downregulated in the Mo group when compared with the NaCl group, whereas minoxidil has no such effect. These results suggest that molybdenum promotes hair growth in a different manner than minoxidil, namely by downregulating hair follicle oxidative stress.

To clarify the link between the antioxidant effect of molybdenum and the accelerated hair growth of the Mo group, we performed RNA sequencing on the experimental samples. When analyzing the differential genes between the Mo group and the NaCl group, we found that the gene Srd5a2 related to male pattern baldness was up-regulated in the Mo group. Srd5a2 is a gene that encodes an enzyme involved in the conversion of testosterone to dihydrotestosterone (DHT), which is known to play a role in androgenetic alopecia. DHT leads to hair follicle atrophy and eventual hair loss through activation of the androgen receptor (AR). Therefore, upregulation of DHT levels may contribute to hair loss through regulation of Srd5a2. Therefore, we also assessed the expression of AR. The results showed that the expression of AR was down-regulated in Mo group. This result could explain why even elevated levels of Srd5a2 did not negatively affect hair growth in mice. Even with the ability to increase DHT levels, the additional DHT produced may not be fully utilized due to low levels of AR expression.

Oxidative stress may lead to the activation of various inflammatory factors. In our data, we observed a significant downregulation of Il1f8 in Group Mo. Interleukin-1 family member 8 (IL1F8), an IL-36beta-related cytokine, is involved in inflammation and immune responses and has been shown to promote inflammation and oxidative stress in various cell types. We propose that IL1F8 induces oxidative stress in hair follicles by activating the NF-κB pathway, leading to the production of pro-inflammatory cytokines and reactive oxygen species. Therefore, molybdenum may promote hair growth by down-regulating Il1f8 in an antioxidant manner.

Overall, oxidative stress is one of the key factors that contribute to hair loss, and molybdenum plays a key role in reducing oxidative stress and protecting against hair loss. The possible mechanism is that molybdenum can down-regulate oxidation factors including iNOS, COX2, Il1f8, and up-regulate the number of CD34 and HFSCs. In addition, molybdenum may promote the occurrence of AGA by down-regulating Ar. Mo NPs can accelerate hair growth and density in mice as observed in a mouse model of hair loss. All these suggest that Mo NPs may be a potential solution for the treatment of hair loss through its antioxidant effect.

Compared with the prior art, the present invention has positive and obvious technical effects. The molybdenum nanoparticles selected in the present invention may promote hair growth by down-regulating ROS, and nanoscale molybdenum can accelerate hair growth, increase the number of local hair follicles, and reduce the expression of molecules related to oxidative stress, such as iNOS, COX2, and androgen receptor. Our study demonstrates that nanoscale molybdenum is a potential topical drug for the treatment of hair loss by inhibiting oxidative stress pathways.

Description of drawings

Figure 1 shows the characterization of molybdenum nanoparticles; (A) shows a representative image of the substance used to treat mice. From left to right, normal saline (NaCl), minoxidil, and molybdenum stock solution. (B) shows a transmission electron microscope (TEM) image of molybdenum nanoparticles, and the scale bar indicates a length of 200 nm. (C) shows the X-ray photoelectron spectroscopy (XPS) spectrum of molybdenum, with oxygen, carbon, and silicon as reference spectra for comparison.

Figure 2 shows the comparison of hair growth and length observed in mice under different treatments. (A) Representative photographs showing the dorsal skin condition of mice under different treatments, photographs were taken on days 1, 4, 7, 10, 13 and 16, respectively. (B) Representative photographs of hair length measurements in mice at day 16. (C) Hair length was compared between the five groups at day 16. (D) Representative microscopic images of the dorsal skin of different groups of mice at days 4, 7, 10, and 13. (E) Comparison of hair density among the five groups. Data are presented as mean ± standard deviation (SD), n = 5 mice per group. *p<0.05, **p<0.01, ***p<0.001 are significantly different from the indicated groups.

Figure 3 (A-E) are the control group (Group Con), normal saline group (Group NaCl), minoxidil group (Group Mi), Mo nanoparticle group (Group Mo) and minoxidil+Mo nanoparticle group (Group MM) Hematoxylin and eosin (HE) stained images of skin tissue sections. (F) Quantitative analysis of the number of hair follicles in the low power field (LPF) of each group. Legend indicates 100 μm. Data are presented as mean ± standard deviation (SD), n = 5 mice per group. *p<0.05, **p<0.01, ***p<0.001 means that the difference with the specified group is statistically significant.

Figure 4 shows the immunohistochemical staining of iNOS and COX2 in the back skin of mice in different treatment groups. (A) Representative images (10 times magnification) of iNOS and COX ₂ immunohistochemical staining in the back skin of mice in each group, arranged in left and right columns from top to bottom, respectively. The scale bar represents 100 μm. (B) Comparison and statistical analysis of iNOS AOD per hair follicle in each group. (C) Comparison and statistical analysis of COX2AOD per hair follicle in each group. Data are expressed as mean ± standard deviation (SD), 5 mice per group. *p<0.05, **p<0.01, ***p<0.001 are significant compared with NaCl group.

Figure 5 shows the results of immunohistochemical staining of CD34 in the skin of different mouse groups. From left to right, the upper row shows the CD34 immunohistochemical staining results of Con group, NaCl group, Mi group, Mo group and MM group. The images of the NaCl group and the Mo group are enlarged in the lower row, and the blue arrows indicate CD34 positive staining. The rightmost panel shows the statistical comparison of CD34AOD values per hair follicle for the five groups. Data are presented as mean ± standard deviation (SD), n = 5 mice per group. *p<0.05, **p<0.01, ***p<0.001 are significantly different from Con group or NaCl group. Scale bar for all panels is 100 μm.

Figure 6 shows the results of RNAseq analysis of mouse skin samples treated with different treatment regimens. (A) 3DPCA plot showing variance of contribution of different treatments for five groups (n=3 for each group but n=4 for group MM). (B) Bar graph showing the number of differential genes between Mo group and NaCl group. (C) Volcano plot showing differential genes between Mo group and NaCl group, up-regulated genes are shown in red, down-regulated genes are shown in blue, and the top ten genes are labeled. (D-F) Bar graphs showing the FPKM expression levels of Srd5a2, AR and Il1f8, respectively.

Detailed ways

Example 1 mouse

All animal experiments were approved by the Experimental Animal Welfare and Ethics Management Committee of Shanghai Dongfang Hospital. 7-week-old male C57BL/6 mice (from Shanghai JSJ Experimental Animal Company) were divided into five groups. The Mi group received 0.1 ml of 5% (mass volume percent concentration) minoxidil (Shanxi Zhendong Health Industry Group, China) on their backs every day. The Mo group received a daily treatment of 0.1 ml of nanomolybdenum solution (33 ppm) dissolved in normal saline on their backs. The NaCl group received 0.1 ml of normal saline on their backs daily, while the Con group received no treatment. The MM group received daily treatment of minoxidil (0.1 ml) and nanomolybdenum solution (0.1 ml) dissolved in normal saline on their backs. The mice were depilated with a mixture of rosin and wax, and petroleum jelly was applied after depilation until the mice in all groups entered the telogen phase of the hair follicles. Before depilation and photographing, all mice were anesthetized with intraperitoneal injection of pentobarbital sodium (1 mg/day) and kept warm. When required, mice were euthanized by cervical dislocation and dorsal skin samples were collected for HE, IHC and RNAseq analysis.

The synthesis of embodiment 2 molybdenum nanoparticles

Molybdenum nanoparticles were prepared by mechanical exfoliation of 6 g of molybdenum powder (Macklin) in a mixture of 100 ml of isopropanol (Macklin) at 450 W and 75% duty cycle for 20 h. Collect the supernatant and remove the isopropanol using a rotary evaporator. The prepared molybdenum nanoparticles were dispersed and dissolved in saline, and the concentration was adjusted to 33ppm.

Characterization of Mo nanoparticles:

Mo nanoparticles were synthesized by mechanical exfoliation of Mo powder and isopropanol. The overall appearance of the applied substances of normal saline (NaCl), minoxidil and Mo nanoparticle solutions from left to right is shown in Fig. 1A. The visual differences of the three treatments were obvious, the NaCl group was colorless, the Minoxidil group had a slight yellow tinge, while the Mo nanoparticle solution had a dark blue-black tinge. These observations are consistent with the physical properties of the respective substances. It should be noted that the color of the Mo nanoparticles solution may be caused by its unique chemical composition and particle size, which were further characterized by transmission electron microscopy and X-ray diffraction analysis, as shown in Figures 1B and 1C. TEM analysis showed that the size of the prepared Mo nanoparticles was about 50 nm (Fig. 1B). The XPS spectrum showed that the Mo 3d peak of the nanoparticles started at 227.80 eV and ended at 241.80 eV (Fig. 1C).

Embodiment 3 Experimental device

Transmission electron microscopy (TEM) images were acquired using a FEI Talos F200X instrument, while X-ray photoelectron spectroscopy (XPS) spectra were collected using a ThermoFisher Scientific ESCALAB 250XI system.

Embodiment 4 histological examination

To assess skin morphology and hair regrowth, skin samples were collected on day 16, fixed in 4% paraformaldehyde for 24 hours, and embedded in paraffin blocks. Hair follicle cross-sections or longitudinal sections of 5 μm thickness were prepared and stained with hematoxylin and eosin (HE staining). Photographs of HE-stained sections were taken using a light microscope. Count the number of hair follicles in each sample using a low power microscope.

Example 5 Immunohistochemical staining

Paraffin sections were dewaxed to water, using environmentally friendly dewaxing agent (three tanks of 10 min, 10 min, 10 min), gradient alcohol (anhydrous, 95%, 75%) for 5 min in each tank, and washed with TBS 3 times, each for 3 minutes. Then, add antigen retrieval solution PH9.0 EDTA retrieval solution to the autoclave, the volume of the retrieval solution should cover the section. Put the lid on the induction cooker and heat until boiling (2100 watts for the induction cooker). Put the dewaxed and hydrated tissue slices into the boiling buffer solution, close the lid tightly, wait for a while to lift the gas nozzle, add a pressure limiting valve (adjust the power of the induction cooker to 800-1200 watts), and wait until the pressure cooker is sprayed. Time for 1min30s, then stop the fire; pour cold water on the pressure cooker, open the lid after the air pressure drops, and wait for the repair solution to cool down to room temperature (25-30°C) (about 1hr), take the slices out of the repair solution, wash with TBS (5min× 3 times) Soak. After cooling (after rewarming), the slices were taken out and soaked in TBS for 3 minutes, then soaked in 3% H ₂ O ₂ for 30 minutes at room temperature. Use a histochemical pen to draw a circle outside the specimen and place it in TBST, then add 10% goat serum dropwise and incubate at room temperature for 30 minutes. The serum was discarded, and iNOS (BA0362, Boster, 1:1000), COX2 (BA0738, Boster, 1:150) and CD34 (Abcam, ab81289, 1:1000) were used as primary antibodies. The primary antibody was diluted with 10% goat serum, and 50ul of different primary antibodies were added dropwise to each section, and incubated overnight at 4°C. The next day, take the slices out of the refrigerator and place them at room temperature for 15 minutes, wash them with TBST three times, then soak them three times for three minutes each time, shake off the TBST, add secondary antibody to each slice and incubate at 37°C for 45 minutes, wash with TBST for 3 minutes. times, three minutes each time. Subsequently, TBST was removed, and 50ul (depending on the size of the tissue) freshly prepared DAB was added dropwise to each slice, observed under a microscope, timed, and tap water to terminate the reaction. Stain the nuclei with hematoxylin for 1 min, wash, differentiate with hydrochloric acid and alcohol for 1-2 seconds, wash, and wash after the bluing solution turns blue for a few seconds, and then observe the staining of the nuclei under a microscope. Seal the slides with an environmental-friendly mountant, dry them, and examine them under a microscope. Store in a dry and cool place at room temperature. White light microscope examination took pictures and recorded, and then used iNOS (BA0362, Boster, 1:1000), COX ₂ (BA0738, Boster, 1:150) and CD34 (Abcam, ab81289, 1:1000) as primary antibodies. IHC staining analysis was performed using the Image J IHC toolbox.

In IHC staining, iNOS and COX ₂ expression levels of Group Mo were reduced

As mentioned before, Mo lowering ROS may play a role in promoting hair growth. iNOS23 and COX ₂ are two molecular markers closely related to oxidative stress. In this study, we performed IHC staining for iNOS and COX ₂ on skin samples from all five experimental groups (Fig. 4A). The results showed that the iNOS AOD per hair follicle in Group Mo was the lowest (0.00096±0.00029), significantly different from the other four groups, and significantly different from Group NaCl (0.00262±0.00040) (Fig. 4B). Also, the COX ₂ AOD per hair follicle in Group Mo (0.00111±0.00020) was the lowest among all groups, and there was a significant difference from Group NaCl (0.00210±0.00124) (Fig. 4C).

Example 6 RNA isolation and library preparation

Total RNA was extracted using TRIzol reagent (Invitrogen, CA, USA) following the manufacturer's protocol. The purity and concentration of RNA were determined using a NanoDrop 2000 spectrophotometer (Thermo Scientific, USA). RNA integrity was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA). Subsequently, libraries were constructed using the VAHTS Universal V RNA-seq library preparation kit following the manufacturer's instructions. OE Biotech Co., Ltd. (Shanghai, China) performed transcriptome sequencing and analysis.

Example 7 RNA sequencing and analysis of differentially expressed genes

The library was sequenced using the Illumina Novaseq 6000 platform to generate 150bp paired-end reads. Use fastp18 to process raw reads in fastq format, remove low-quality reads to obtain clean reads. Clean reads were mapped to a reference genome using HISAT19. The expression level of each gene was calculated using FPKM20, and the read count of each gene was obtained using HTSeq-count21. To assess the biological reproducibility of the samples, PCA analysis was performed using R (v 3.2.0). Differential expression analysis was performed using DESeq222, and Q value <0.05 and fold change rate >2 or fold change rate <0.5 were set as thresholds for significantly differentially expressed genes (DEGs). Hierarchical cluster analysis was performed using R (v3.2.0) to show the expression patterns of genes in different groups and samples. A radar map of the top 10 genes of upregulated or downregulated DEGs was displayed using the R package ggradar.

RNAseq analysis showed down-regulation of ROS-related genes in the Mo group:

RNAseq analysis was performed on skin samples from mice with different treatment regimens on day 16. The 3D PCA plot (Fig. 6A) showed that the different treatment regimens resulted in differences among the five experimental groups, three mice were analyzed for each group, except the MM group. In the differential gene analysis between the NaCl group and the Mo group, 149 up-regulated genes and 1027 down-regulated genes were identified (Fig. 6B). Differential gene expression analysis was visualized in a volcano plot (Figure 6C), where each point represents a gene and is colored according to the direction of regulation. The top ten generics include Mup19, Mup18, Aire, GM52481, AMTN, SRD5A2, ALFM3, Gab12, Gabre and B3Gnt7, and the first ten generic reduction genes include IL1F8, SPRR2A2, KLRA1, GML2, MC3R, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3,, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3, KCNJ3. Ggcy2fl541, GM22798 and Spink7. Through DESeq analysis, it was found that ROS-related genes, including Nos1, Nos1ap, Nos2 (associated with iNOS), and Ptgs1 and Ptgs2 (associated with COX2), were down-regulated in the Mo group compared with the NaCl group (Table 1). The expression of Srd5a2 was upregulated in Mi group, Mo group and MM group, compared with Con group and NaCl group (Fig. 6D), while the expression of its target receptor Ar was downregulated in Mo group (Fig. 6E). The gene Il1f8 related to inflammation and oxidative stress was specifically downregulated in the Mo group (Fig. 6F).

Table 1. DESeq results comparing Nos1, Nos1ap, Nos2, Ptgs1 and Ptgs2 gene expression between Mo group and NaCl group.

Embodiment 8 hair length analysis

Five mice were selected from each group, and at least 50 hairs were collected from each mouse. The length of the hair was measured using a vernier caliper (Deli Group).

Embodiment 9 statistical analysis

Statistical analysis was performed using Prism 9.0 (GraphPad Software). Results are reported as mean ± standard deviation (SD). Statistical tests used, number of animals and P-values are described in the legend of each figure or represented as dots in the figure.

Embodiment 10 hair density analysis

Hair density was assessed using a microscope (Beining Co., Ltd., Nanjing, China). The microscope was placed at a distance of approximately 2-3 cm from the skin on the back of the mouse. Hair density was assessed by counting the number of hair follicles per unit area, usually expressed as hairs per square centimeter with software (Beining Co., Ltd., Nanjing, China).

Mo nanoparticles accelerated hair growth in mice:

Observe the condition of the back skin of the treated mice after different substance treatments, and record the photos of the 1st, 4th, 7th, 10th, 13th and 16th days. On the 7th day, the skin color of the Mi group, the Mo group, and the Minoxidil and Mo nanoparticle combination treatment group (MM group) became darker, while the skin color of the control group and the NaCl group turned darker later, and did not turn black until the 10th day (Fig. 2A). On day 16, there was no significant difference in hair length between the Con group (4.02±0.13) and the NaCl group (4.20±0.13). However, the hair length of Mi group (6.82±0.17), Mo group (6.72±0.26) and MM group (7.12±0.15) was significantly higher than that of NaCl group (Fig. 2B and 2C). In addition, the MM group had the longest hair length among the five groups. Hair growth was assessed using dermoscopy, and the results showed that the hair density of the MM group first reached more than 600/cm ² (669.16±12.03) on day 4 (Fig. 2D). In addition, there was a significant difference in hair density between the Mi group (3502.25±172.80) and the MM group (4240.22±336.36) on day 13. In addition, the hair density of the Mo group (3550.46 ± 136.41) was lower than that of the MM group, and there was no significant difference compared with the Mi group (Fig. 2E).

The number of hair follicles increased in the Mo-treated group:

Skin samples from different groups of mice were examined histologically for hematin and eosinophil staining (Figure 3A-E). The number of hair follicles in low power field (LPF) was counted and analyzed. The results showed that there was no significant difference in the number of hair follicles in the Con group (20±1) and the NaCl group (21±3), while the Mi group (28±1), the Mo group (31±3) and the MM group (31±4) The number of hair follicles in was significantly increased compared with the Con group and the NaCl group (Fig. 3F).

CD34+ hair follicle stem cells were upregulated in the Mo group:

CD34+ hair follicle stem cells 25 are a type of stem cell that resides in the hair follicle and plays an important role in hair growth. These cells are responsible for generating new hair follicles and maintaining the growth and regeneration of existing hair follicles. To investigate whether CD34+ hair follicle stem cells might be associated with hair growth-promoting upregulation in the Mo group, we performed CD34+ immunohistochemical staining on all five groups. The results showed that the CD34 AOD per hair follicle was the highest in the MM group (0.00253±0.00076). The expression of CD34AOD per hair follicle was higher in the Mo group (0.00201 ± 0.00024), which was significantly different from that in the NaCl group (0.00111 ± 0.00030) (Fig. 5).

Claims (5)

1. The use of molybdenum nanoparticles in the preparation of medicines for treating hair growth. 2. The use according to claim 1, characterized in that the molybdenum nanoparticles are nanoscale molybdenum monomers. 3. The use according to claim 2, characterized in that the molybdenum nanoparticles are dissolved in physiological saline for use. 4. A pharmaceutical composition for treating hair growth, characterized in that it consists of molybdenum nanoparticles and minoxidil. 5. Use of the combination of molybdenum nanoparticles and minoxidil in the preparation of a medicament for treating hair growth.

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