Application of glabridin in preparation of related drugs for inhibiting epithelial-mesenchymal transition

Abstract

The invention discloses an application of glabridin in preparation of related drugs for inhibiting epithelial-mesenchymal transition in inflammatory bowel diseases. In the epithelial-mesenchymal transformation process, epithelial cells lose cell polarity and intercellular connection, are transformed into mesenchymal cells in function and morphology, directly participate in fibroblast activation and extracellular matrix deposition and cause intestinal fibrosis, and are one of anti-fibrosis targets. According to the application of the glabrione in preparation of the medicine related to inhibition of epithelial-mesenchymal transition in the inflammatory bowel disease, provided by the invention, the expression change of epithelial cell markers Claudin-1 and E-cadherin caused by TGF-beta 1 and interstitial cell markers Vimentin, N-cadherin, Snail and alpha-SMA can be relieved, cell migration caused by TGF-beta is improved, and the epithelial-mesenchymal transition induced by TGF-beta 1 is inhibited. The research on the mechanism of action shows that by blocking a TGF-beta1 / Smad2 / 3 signal channel and inhibiting AKT1 activation and inhibition of epithelial-mesenchymal transition, the application of the compound in inhibition of epithelial-mesenchymal transition and prevention of intestinal disease related fibrosis is prompted.

Description

Technical Field

[0001] The present invention relates to the technical field of medicine, specifically to the technical field of application of flavonoids in the preparation of relevant medicines, and more specifically to the technical field of application of glabridin in the preparation of medicines related to inhibiting epithelial-mesenchymal transition. Background Art

[0002] Epithelial-mesenchymal transition (EMT) is one of the important mechanisms of intestinal fibrosis. In this process, epithelial cells lose cell polarity and intercellular connections, epithelial cell markers such as Claudin and E-cadherin gradually disappear, and mesenchymal cell markers such as N-cadherin and Snail gradually increase. They are functionally and morphologically transformed into mesenchymal cells, directly participating in fibroblast activation and extracellular matrix deposition. In addition, damaged epithelial cells are an important source of fibroblasts and promote organ fibrosis through epithelial-mesenchymal transition in different fibrotic tissues. Therefore, epithelial-mesenchymal transition is considered to be one of the therapeutic targets for intestinal fibrosis. The occurrence of epithelial-mesenchymal transition is related to a variety of cytokines, protein molecules, microenvironment, etc., involving a large number of cell signaling pathways and complex gene regulation processes. Among them, the TGF-β / Smad3 pathway is the most classic and important epithelial-mesenchymal transition pathway, and studies have also confirmed that this pathway also plays a vital role in promoting intestinal fibrosis.

[0003] EMT not only plays a role in normal physiological processes such as embryonic development and tissue regeneration, but is also associated with carcinogenesis and confers metastatic properties to cancer cells by enhancing mobility, invasiveness, and resistance to apoptotic stimuli. In addition, tumor cells derived from EMT acquire stem cell properties and exhibit significant therapeutic resistance. Given these properties, EMT is considered a key hallmark of carcinogenesis, and targeting EMT has become one of the strategies for cancer treatment.

[0004] The prior art reports that licochalcone A is an active ingredient that inhibits epithelial-mesenchymal transition of human osteosarcoma cells, liver cancer cells, and oral cancer cells (Chen Meikai. Study on licochalcone A inducing apoptosis of human osteosarcoma cells and inhibiting epithelial-mesenchymal transition through Wnt / β-catenin signaling pathway [D]. Hangzhou: Zhejiang University, 2020; Shen Huan, et al. Anti-timetastatic effects of licochalcone A on oral cancer via regulatingmetastasis-associated proteases [J]. Tumour Biol, 2014, 35(8): 7467-74.). Summary of the invention

[0005] The purpose of the present invention is to provide an effective ingredient that plays a better role in inhibiting epithelial-mesenchymal transition, and to provide the use of licorice in the preparation of drugs that inhibit epithelial-mesenchymal transition, especially through the TGF-β / Smads pathway and the AKT signaling pathway to inhibit epithelial-mesenchymal transition. The use of licorice in the preparation of drugs that inhibit epithelial-mesenchymal transition provided by the present application can alleviate the expression changes of epithelial cell markers Claudin-1, E-cadherin, and mesenchymal cell markers Vimentin, N-cadherin, Snail, and α-SMA caused by TGF-β1, improve cell migration caused by TGF-β, and inhibit TGF-β1-induced epithelial-mesenchymal transition. Mechanism of action studies have shown that it inhibits epithelial-mesenchymal transition by blocking the TGF-β1 / Smad2 / 3 signaling pathway and inhibiting AKT1 activation, suggesting its value in inhibiting epithelial-mesenchymal transition and preventing intestinal disease-related fibrosis.

[0006] In order to achieve the above technical effects, the present invention is implemented through the following technical solutions.

[0007] The present application provides the use of glabridin or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition.

[0008] The medicine comprises glabridin or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable adjuvant.

[0009] The glabridin or a pharmaceutically acceptable salt thereof inhibits epithelial-mesenchymal transition via the TGF-β / Smads pathway and the AKT signaling pathway.

[0010] The pharmaceutically acceptable salts include salts formed between glabridin and pharmaceutically acceptable acids or bases.

[0011] The drug is suitable for oral, rectal, nasal, topical, parenteral administration.

[0012] The medicine is one of tablets, powders, granules, pills, capsules, solutions, emulsions, suspensions, oils, sprays, injections, suppositories, liposome preparations, microparticle preparations, and microcapsule preparations.

[0013] In the drug, the amount of glabridin or its pharmaceutically acceptable salt is 0.01% to 50% of the total weight.

[0014] The present application also provides a drug for inhibiting epithelial-mesenchymal transition, the drug comprising glabridin and a drug with glabridin as the active ingredient.

[0015] The medicine comprises glabridin and medically acceptable auxiliary materials.

[0016] By implementing the above specific technical solutions provided by the present invention and implementing the content of the present invention, the following beneficial effects can be obtained: (1) The licorice ketone provided in this application can alleviate the inflammatory response caused by TNF-α, inhibit the expression changes of epithelial cell markers Claudin-1 and E-cadherin, and mesenchymal cell markers Vimentin, N-cadherin, Snail, and α-SMA caused by TGF-β1, improve cell migration caused by TGF-β, and inhibit TGF-β1-induced epithelial-mesenchymal transition. Mechanism studies have shown that it inhibits epithelial-mesenchymal transition by blocking the TGF-β1 / Smad2 / 3 signaling pathway and inhibiting AKT1 activation, suggesting its value in inhibiting epithelial-mesenchymal transition and preventing intestinal disease-related fibrosis.

[0017] (2) The present application provides the use of licorice root or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition, wherein IEC-6 cells in the logarithmic growth phase are taken, and after TNF-α stimulation, IL-6 secretion is significantly increased ( P <0.05), indicating an inflammatory response. 10 and 20 μg / ml of glabrata ketone significantly reduced the level of IL-6 ( P <0.05), and the inhibitory effect of 20μg / ml of licorice root on IL-6 secretion was significantly different from that of the positive drug sulfasalazine ( P <0.05).

[0018] (3) The present application provides the use of licorice root or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition, and 2.5 μM licorice root significantly increases the expression level of E-cadherin ( P <0.05), 5μM licorice root significantly increased the expression levels of Claudin-1 and E-cadherin ( P <0.05). In addition, the effect of 5μM licorice chalcone on regulating Claudin-1 was significantly different from that of 2.5μM licorice chalcone A ( P <0.05), the effect of regulating E-cadherin was significantly different from that of 2.5 and 5 μM licorice chalcone A ( P <0.05). It is proved that the glabridin in the technical solution provided by the present application has better activity than licochalcone A in inhibiting the loss of epithelial cell characteristics in epithelial-mesenchymal transition.

[0019] (4) The present application provides the use of 5 μM licorice root or its pharmaceutically acceptable salt in the preparation of a drug for inhibiting epithelial-mesenchymal transition. The provided 5 μM licorice root significantly inhibits the expression of vimentin and N-cadherin ( P <0.05), 2.5 and 5 μM of licorice significantly inhibited the expression of Snail and α-SMA ( P <0.05), indicating that the licorice root provided in the technical solution of the present application has an inhibitory effect on the epithelial-mesenchymal transition caused by TGF-β1.

[0020] (5) The present application provides the use of licorice root or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition, which significantly promotes the increase of cell migration rate through TGF-β1 stimulation ( P <0.05), indicating that it increases the invasion and migration ability of IEC-6 cells. The technical solution provided by this application 5μM of glabrata significantly inhibits the increase in cell migration rate caused by TGF-β1 ( P <0.05), further indicating that licorice root can inhibit epithelial-mesenchymal transition.

[0021] (6) The present application provides the use of licorice root or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition, which significantly inhibits the fluorescence intensity of E-cadherin ( P <0.05), improve the fluorescence intensity of Vimentin ( P <0.05). The technical solution provided by this application, 5 μM of licorice root, significantly inhibited the changes in the fluorescence intensity of E-cadherin and Vimentin caused by TGF-β1 ( P <0.05), the expression of intercellular E-cadherin and Vimentin was significantly enhanced compared with the model group.

[0022] (7) The present application provides the use of licorice root or its pharmaceutically acceptable salt in the preparation of a drug for inhibiting epithelial-mesenchymal transition. After stimulation by TGF-β, the phosphorylation of Smad2, Smad3, and AKT1 is significantly increased ( P <0.05), the technical solution provided by this application, licorice ketone, significantly inhibited the activation of these three proteins ( P <0.05), suggesting that licorice may inhibit epithelial-mesenchymal transition and prevent intestinal fibrosis by inhibiting the activation of TGF-β / Smad signaling pathway and AKT signaling pathway. BRIEF DESCRIPTION OF THE DRAWINGS

[0023] Figure 1 Shown is the result of the effect of licorice root and licorice chalcone A on the survival rate of IEC-6 cells.

[0024] Figure 2 Shown is the result of the effect of licorice root and licorice chalcone A on the inflammatory response caused by TNF-α.

[0025] Figure 3 Shown is the effect of licorice root and licorice chalcone A on the change of Claudin-1 expression induced by TGF-β1.

[0026] Figure 4 Shown is the effect of licorice root and licorice chalcone A on the change of E-cadherin expression caused by TGF-β1.

[0027] Figure 5 Shown is the effect of licorice root on Vimentin expression.

[0028] Figure 6 Shown is the result of the effect of licorice root on the expression of N-cadherin.

[0029] Figure 7 Shown is the result of the effect of licorice root on the expression of Snail.

[0030] Figure 8 Shown is the result of the effect of licorice root on the expression of α-SMA.

[0031] Fig. 9 Shown is the Western Blot detection result.

[0032] Fig.10 Shown is the result of the effect of licorice root on cell migration.

[0033] Fig.11 Shown are the results of cell migration experiments.

[0034] Fig.12 Shown is the result of the effect of licorice root on the fluorescence intensity of E-cadherin.

[0035] Fig.13 Shown is the result of the effect of licorice root on the fluorescence intensity of Vimentin.

[0036] Fig.14 Shown is the result of immunofluorescence detection.

[0037] Fig.15 Shown is the result of the effect of licorice root on Smad2 expression.

[0038] Fig.16 Shown is the result of the effect of licorice root on the expression of p-Smad2.

[0039] Fig.17Shown is the result of the effect of licorice root on the expression of Smad3.

[0040] Fig.18 Shown is the result of the effect of licorice root on the expression of p-Smad3.

[0041] Fig.19 Shown is the result of the effect of licorice root on the expression of p-AKT1.

[0042] Fig. 20 Shown is the Western Blot detection result. DETAILED DESCRIPTION

[0043] The present invention is described below with reference to the following examples, but the present invention is not limited to the following examples. All raw and auxiliary materials used in the present invention are well known in the art, and the % involved in the present invention is the mass volume percentage unless otherwise specified.

[0044] Materials: Licorice ketone, licorice chalcone, fetal bovine serum (FBS), DMEM (high glucose) medium, penicillin-streptomycin double antibody (10000U), trypsin (0.25% Trypsin-EDTA), CCK-8 cell proliferation / toxicity detection kit, recombinant human insulin, Recombinant Human TGF-beta 1 Protein, Easy II Protein Quantitative Kit, RIPA lysis buffer, protease inhibitors, goat anti-rabbit IgG H&L (HRP), goat anti-mouse IgG H&L (HRP), SuperSignal™ West Pico PLUS Chemiluminescent Substrate, beta-Actin Loading Control antibody Mouse MAb, Anti-E Cadherin antibody [4A2], Anti-Claudin 1 Antibody, Recombinant Anti-Vimentin antibody [EPR3776]- Cytoskeleton Marker, Rabbit Anti-N-cadherinantibody, Snail (C15D3) Rabbit mAb, Rabbit Anti-alpha smooth muscle Actinantibody, Smad2 (D43B4) XP® Rabbit mAb #5339, Phospho-Smad2 (Ser465 / 467)(138D4) Rabbit mAb #3108, Smad3 (C67H9) Rabbit mAb #9523, Phospho-Smad3(Ser423 / 425) (C25A9) Rabbit mAb #9520, Phospho-Akt (Ser473) (D9E) XP® Rabbit mAb #4060, Goat anti-rabbit IgG H&L (Alexa Fluor® 488), DAPI, Goat anti-mouse IgG H&L (Alexa Fluor® 488).

[0045] Instruments: CO2 cell culture incubator, desktop low-speed centrifuge, fluorescence inverted microscope, microplate reader, confocal microscope, chemiluminescence imaging system, protein transfer instrument, electrophoresis instrument, micro-spectrophotometer.

[0046] In order to better explain the present invention, the main contents of the present invention are further illustrated below in conjunction with specific examples, but the contents of the present invention are not limited to the following examples. Unless otherwise specified, the technical means used in the examples are conventional means well known to those skilled in the art, and the raw materials used are all commercially available commodities.

[0047] Example 1: Use of licorice root or its pharmaceutically acceptable salt in the preparation of drugs for inhibiting epithelial-mesenchymal transition The present application provides the use of glabridin or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition.

[0048] The glabridin or a pharmaceutically acceptable salt thereof inhibits epithelial-mesenchymal transition via the TGF-β / Smads pathway and the AKT signaling pathway.

[0049] The pharmaceutically acceptable salts include salts formed between glabridin and pharmaceutically acceptable acids or bases.

[0050] In the drug, the effective amount of glabridin or a pharmaceutically acceptable salt thereof is 2.5-5 μM.

[0051] The present application also provides a drug for inhibiting epithelial-mesenchymal transition, the drug comprising glabridin and a drug with glabridin as the active ingredient.

[0052] Example 2: Determination of cell viability IEC-6 cells with good growth and confluence of 90% were obtained, digested with trypsin, and prepared into 5×10 4 cells / mL single cell suspension was inoculated into a 96-well plate (100μL / well). After culturing at 37℃ and 5% CO2 for 24h, the culture medium was discarded and 100μL of 10 and 20μg / ml glabridin and licorice chalcone A solutions were added respectively. At the same time, a blank group was set up for intervention for 48h (n=5). After the intervention, the culture medium was discarded and 100μL of 10% CCK-8 solution was added to each well. The cells were continued to be incubated in the incubator. After 1h, the OD value at 450nm was measured with an enzyme reader to detect the cell survival rate. The results of the measurement are shown in the attached Figure 1 As shown, after intervention with 10 and 20 μg / ml of licorice root and licorice chalcone A, the cell survival rate was >85%, and this concentration can be used for subsequent experiments.

[0053] Example 3: Detection of Inflammation Inhibition Based on the above examples, IEC-6 cells in the logarithmic growth phase were taken and blank group, TNF-α (100 ng / ml) intervention group, positive control group (2 mM sulfasalazine intervention 2 h in advance), drug intervention group (10, 20 μg / ml glabridin, licorice chalcone A intervention 2 h in advance) (n=3) were designed. The intervention time was 24 h. After the end, the cell supernatant was collected and the IL-6 level was detected by ELISA. The results of the determination are shown in the attached Figure 2 As shown in the results, IL-6 secretion increased significantly after TNF-α stimulation ( P <0.05), indicating an inflammatory response. 10 and 20 μg / ml of licorice and licorice chalcone A can significantly reduce the level of IL-6 ( P <0.05), and the inhibitory effect of 20μg / ml of licorice root on IL-6 secretion was significantly different from that of the positive drug sulfasalazine ( P <0.05).

[0054] Example 4: Effects on epithelial cell markers IEC-6 cells in the logarithmic growth phase were taken and designed into a blank group, a TGF-β1 intervention group (10 ng / mL), and a TGF-β1 intervention + drug intervention group (2.5, 5 μM, glabridin and licorice chalcone A 30 min in advance) (n=3). The intervention time was 48 h. After the end, the cells were collected and the protein concentration was determined. Western Blot was used to detect the content of Claudin-1 and E-cadherin. The results of the determination are shown in the attached Figure 3 , Attachment Figure 4 As shown in the results, TGF-β1 stimulation can significantly reduce the expression of epithelial cell markers Claudin-1 and E-cadherin ( P <0.05). 2.5μM licorice root significantly increased the expression level of E-cadherin ( P <0.05), 5μM licorice root significantly increased the expression levels of Claudin-1 and E-cadherin ( P <0.05), Licorice Chalcone A only significantly increased the expression level of E-cadherin at a concentration of 5 μM ( P <0.05). In addition, the effect of 5μM licorice chalcone on regulating Claudin-1 was significantly different from that of 2.5μM licorice chalcone A ( P <0.05), the effect of regulating E-cadherin was significantly different from that of 2.5 and 5 μM licorice chalcone A ( P <0.05). This indicates that licorice root has better activity than licorice chalcone A in inhibiting the loss of epithelial cell characteristics in epithelial-mesenchymal transition.

[0055] Example 5: Determination of the effect of TGF-β1 on epithelial-mesenchymal transition Based on the above examples, IEC-6 cells in the logarithmic growth phase were taken and set up as blank group, TGF-β1 intervention group (10 ng / mL), TGF-β1 intervention + drug intervention group (2.5, 5 μM, glabrata ketone intervention 30 min in advance) (n=3), intervention time 48h, after which cells were collected, protein concentration was determined, and Western Blot was used to detect the expression of Vimentin, N-cadherin, Snail, and α-SMA proteins. The results of the determination are shown in the attached Figure 5 , Attachment Figure 6 , Attachment Figure 7 , Attachment Figure 8 , Attachment Fig. 9 As shown, the results showed that TGF-β1 stimulation can significantly increase the expression of mesenchymal cell markers Vimentin, N-cadherin, Snail, and α-SMA ( P <0.05), indicating that it caused epithelial-mesenchymal transition. 5μM of licorice significantly inhibited the expression of Vimentin and N-cadherin ( P <0.05), 2.5 and 5 μM of licorice significantly inhibited the expression of Snail and α-SMA ( P <0.05), indicating that licorice root has an inhibitory effect on epithelial-mesenchymal transition caused by TGF-β1.

[0056] Example 6: Determination of the effect on cell migration induced by TGF-β1 Based on the above examples, IEC-6 cells were prepared with complete culture medium at a density of 1×10 5 cells / mL single cell suspension was inoculated into a 24-well plate (500μL / well). When the cell growth confluence rate reached 100%, the intervention experiment was carried out. Set up a blank group, a TGF-β1 intervention group (10ng / mL TGF-β1 intervention), and a TGF-β1+drug intervention group (5μM licorice ketone intervened in advance for 30 minutes and then used 10ng / mL TGF-β1 intervention) (n=3). Use a 10μL pipette tip to scratch the cells in the well plate vertically with a ruler, wash twice with PBS, remove the scratched cells, and replace the serum-free culture medium according to the group. After 24h, take out the cells to observe the migration of cells, take pictures, and use imageJ software to measure the scratch area to calculate the Wound healing rate (%) to evaluate the cell migration ability. The measurement results are shown in the attached. Fig.10 , Attachment Fig.11 As shown, the results showed that TGF-β1 stimulation significantly promoted the increase of cell migration rate ( P<0.05), indicating that it increased the invasion and migration ability of IEC-6 cells. 5μM of glabrata significantly inhibited the increase in cell migration rate caused by TGF-β1 ( P <0.05), further indicating that licorice root can inhibit epithelial-mesenchymal transition.

[0057] Example 7: Determination of the effect of TGF-β1 on the expression changes of E-cadherin and Vimentin Based on the records of the above examples, the slices of the above cell migration experiment were fixed with 4% paraformaldehyde for 10 minutes, washed with PBS three times, each time for 2 minutes; blocked with 1% BSA at room temperature for 40 minutes, and the blocking solution was dried; 80 μL of 2 μg / mL Anti-E-cadherin and Anti-Vimentin antibodies were added, incubated overnight at 4°C, washed with PBS three times, each time for 2 minutes; 80 μL of 2 μg / mL secondary antibodies goat anti-rabbit IgG H&L and goat anti-mouse IgG H&L were added, incubated at 37°C in the dark for 1 hour, washed with PBS three times, each time for 2 minutes; 80 μL of 1 μg / mL DAPI was added, incubated at room temperature in the dark for 5 minutes, washed with PBS three times, each time for 2 minutes; 50% glycerol was used to seal the slices, and the expression of Anti-E-cadherin and Anti-Vimentin proteins in the non-scratched area was observed with a laser confocal microscope, and the fluorescence intensity was calculated using ImageJ. The measurement results are shown in the attached Fig.12 , Attachment Fig.13 , Attachment Fig.14 As shown, the results showed that TGF-β1 stimulation significantly inhibited the fluorescence intensity of E-cadherin ( P <0.05), improve the fluorescence intensity of Vimentin ( P <0.05). 5μM licorice root significantly inhibited the changes in fluorescence intensity of E-cadherin and Vimentin induced by TGF-β1 ( P <0.05), the expression of intercellular E-cadherin and Vimentin was significantly enhanced compared with the model group.

[0058] Example 8: Determination of the effects on Smad signaling pathway and AKT signaling pathway Based on the records in the above examples, IEC-6 cells in the logarithmic growth phase were taken to set up a blank group, a TGF-β1 intervention group (10 ng / mL), and a TGF-β1 intervention + drug intervention group (5 μM, drug intervention 30 min in advance) (n=3). The intervention time was 48 h. After the intervention, the cells were collected and the protein concentration was determined. Western Blot was used to detect the expression of Smad2, p-Smad2, Smad3, p-Smad3, and p-AKT1 proteins.

[0059] The TGF-β / Smads pathway plays an important role in regulating epithelial-mesenchymal transition and promoting intestinal fibrosis. TGF-β is regarded as the best characterized promoter of epithelial-mesenchymal transition. Inhibition of Smad3 phosphorylation can block the TGF-β / Smads signaling pathway and inhibit epithelial-mesenchymal transition and tissue fibrosis. The AKT signaling pathway also plays a role in epithelial-mesenchymal transition. It is involved in the epithelial-mesenchymal transition of various cancer cells such as intestinal cancer and gastric cancer, and is regulated by TGF-β. Therefore, the inhibitory effect of glycyrrhizin on TGF-β activation of Smad2, Smad3, and AKT1 was also investigated. The results of the assay are shown in the attached. Fig.15 , Attachment Fig.16 , Attachment Fig.17 , Attachment Fig.18 , Attachment Fig.19 , Attachment Fig. 20 As shown, the results showed that after TGF-β stimulation, the phosphorylation of Smad2, Smad3, and AKT1 was significantly increased ( P <0.05), while licorice root significantly inhibited the activation of these three proteins ( P <0.05), suggesting that licorice may inhibit the activation of TGF-β / Smad signaling pathway and AKT signaling pathway, inhibit epithelial-mesenchymal transition and prevent intestinal fibrosis.

[0060] The embodiments described above are only some embodiments of the present invention, not all embodiments. The detailed description of the embodiments of the present invention is not intended to limit the scope of the invention claimed for protection, but only represents selected embodiments of the present invention. All other embodiments obtained without creative work and related deductions and substitutions made by ordinary technicians in the field under the conditions of the concept of the present invention belong to the scope of protection of the present invention.

Claims

1. A use of licorice root or a pharmaceutically acceptable salt thereof in the preparation of a drug for inhibiting epithelial-mesenchymal transition.

2. The use according to claim 1, characterized in that: The medicine comprises glabridin or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable adjuvant.

3. The use according to claim 1, characterized in that: The glabridin or a pharmaceutically acceptable salt thereof inhibits epithelial-mesenchymal transition via the TGF-β / Smads pathway and the AKT signaling pathway.

4. The use according to claim 1, characterized in that: The pharmaceutically acceptable salts include salts formed between glabridin and pharmaceutically acceptable acids or bases.

5. The use according to claim 1, characterized in that: The drug is suitable for oral, rectal, nasal, topical, parenteral administration.

6. The use according to claim 1, characterized in that: The medicine is one of tablets, powders, granules, pills, capsules, solutions, emulsions, suspensions, oils, sprays, injections, suppositories, liposome preparations, microparticle preparations, and microcapsule preparations.

7. The use according to claim 1, characterized in that: In the drug, the effective amount of glabridin or a pharmaceutically acceptable salt thereof is 2.5-5 μM.

8. A drug for inhibiting epithelial-mesenchymal transition, characterized in that: The medicine includes glabridin and the medicine with glabridin as the active ingredient.

9. The drug according to claim 8, characterized in that The medicine comprises glabridin and medically acceptable auxiliary materials.

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