Application of isoflavone compound in preparation of product for preventing and / or treating silicosis

Abstract

The invention discloses an application of an isoflavone compound in preparation of a product for preventing and / or treating silicosis. The isoflavone compound is a compound as shown in a formula 1. The isoflavone compound can effectively relieve pulmonary fibrosis and an epithelial-mesenchymal transition process, so that the isoflavone compound plays an important role in blocking the progress of pulmonary fibrosis. The compound not only can be used for preparing medicines for preventing or treating diseases related to fibrosis and epithelium-mesenchymal transition, but also can be widely applied to the fields of health foods, cosmetics, hygienic disinfection articles and the like.

Description

Technical Field

[0001] The present invention relates to the field of biomedicine technology, and in particular to the use of an isoflavone compound in the preparation of a product for preventing and / or treating silicosis. Background Art

[0002] Silicosis is a chronic lung disease caused by long-term inhalation of silica dust particles. Its main pathological features include pulmonary fibrosis, epithelial-mesenchymal transition (EMT), inflammation, and excessive extracellular matrix deposition. Silicosis is the most common occupational lung disease and poses a serious health threat to high-risk groups such as miners and stone processing workers. With the advancement of industrialization, silicosis has become a major public health issue worldwide.

[0003] The pathogenesis of silicosis is related to the accumulation of silica particles in the lungs. It initially triggers a series of inflammatory reactions that, as these inflammations worsen, ultimately lead to the development of pulmonary fibrosis. When workers are exposed to materials containing free silica in their work environments, tiny silica dust particles are released into the air. Once these particles are inhaled into the lungs, alveolar macrophages continuously attempt to engulf them. However, due to the poor biocompatibility of silica, macrophages are unable to effectively clear these silica dust particles. This leads to the activation of inflammatory cells, ultimately causing fibrosis and the epithelial-mesenchymal transition process.

[0004] The occurrence of silicosis is accompanied by a series of complex processes. Symptoms generally appear gradually after the patient has been exposed to silica for a long time. The main manifestation is that there may be no obvious discomfort in the early stages. However, the continuous inflammatory response process will slowly cause lung tissue damage and pulmonary fibrosis, thereby forming scar tissue. This process gradually affects lung function. The lungs of patients with silicosis usually show a large area of ​​diffusely distributed round or irregular small shadows. The more serious the disease, the more these shadows will increase. As the disease progresses, they merge with each other and the body will experience a series of adverse reactions, such as difficulty breathing, dry cough, chest pain, and weight loss.

[0005] Currently, silicosis is a serious problem and there is no complete cure. The main goal of choosing treatment is to relieve patients' symptoms and improve their quality of life. For patients with dyspnea, drug treatment usually includes bronchodilators, anti-inflammatory drugs and steroids. These drugs can relieve patients' dyspnea symptoms and control inflammatory responses. For patients with more serious conditions, oxygen therapy can improve oxygenation and effectively relieve respiratory discomfort. Pulmonary rehabilitation training is currently believed to be able to effectively improve patients' exercise endurance and quality of life. In extremely severe cases, lung transplantation can be used as a last resort. In addition, the body's age, health status, nutritional level and genetic factors will have a significant impact on the risk of silicosis.

[0006] Isoflavones are a class of naturally occurring plant secondary metabolites, found widely in plants such as soybeans and red clover. Studies have shown that isoflavones have significant antioxidant, anti-inflammatory, anti-fibrotic, and cell signaling pathway-regulating effects, with a high safety profile.

[0007] However, no isoflavone compounds (C 20 H 18 O5) Specific application in the prevention and / or treatment of silicosis. Summary of the Invention

[0008] The present invention aims to overcome the shortcomings of the prior art by providing an isoflavone compound for use in the preparation of products for the prevention and / or treatment of silicosis. The compound can be used as a protective agent to alleviate pulmonary fibrosis and epithelial-mesenchymal transition (EMT) caused by silica dust particles, slowing lung tissue damage. The compound also exhibits inhibitory activity against silica dust-induced cellular oxidative stress and inflammatory responses, effectively ameliorating structural damage to lung tissue following silica dust exposure. It can be used as an active ingredient in pharmaceuticals, health foods, and functional hygiene products for the prevention and treatment of silicosis.

[0009] The technical solution to achieve the above object is: an isoflavone compound is used in the preparation of a product for preventing and / or treating silicosis, wherein the isoflavone compound has the molecular formula C 20 H 18 O5, the structural formula is shown in formula (1):

[0010]

[0011] The isoflavone compounds described above protect lung tissue from damage caused by silica dust particles by inhibiting pulmonary fibrosis and epithelial-mesenchymal transition (EMT). Silicosis is caused by long-term inhalation of silica dust particles, which manifests as lung inflammation, fibrosis, decreased lung function, and changes in cell structure.

[0012] The aforementioned isoflavone compounds are used in silica dust-induced pulmonary fibrosis, which is caused by abnormal activation of the TGF-β1 signaling pathway, leading to abnormal deposition of collagen fibers in lung tissue. Epithelial-mesenchymal transition (EMT) is caused by the loss of epithelial cell characteristics and the acquisition of mesenchymal cell characteristics. Lung injury refers to the phenomena of pulmonary fibrosis, alveolar wall structural destruction, and excessive deposition of extracellular matrix that occur after silica dust exposure.

[0013] Preferably, the protection against pulmonary fibrosis refers to reducing collagen fiber deposition and alleviating the progression of pulmonary fibrosis.

[0014] Preferably, the alleviation of epithelial-mesenchymal transition refers to the weakening of the destruction of epithelial cell characteristics.

[0015] The above-mentioned isoflavone compounds, wherein the effective dose for inhibiting silica dust-induced pulmonary fibrosis is 25 mg / kg to 50 mg / kg, can significantly improve the degree of fibrosis in the lung tissue of mice exposed to silica dust at an effective dose of 25 mg / kg to 50 mg / kg. This is manifested by significantly reducing collagen deposition, significantly inhibiting fibroblast activation, and significantly alleviating the epithelial-mesenchymal transition process.

[0016] The above-mentioned application of isoflavone compounds, wherein the pulmonary fibrosis caused by silica dust includes at least one of lung inflammation, lung tissue fibrosis, decreased lung function, silicosis nodule formation and immune dysfunction caused by silica dust exposure.

[0017] The application of the above-mentioned isoflavone compound, wherein the product includes at least one of medicine, health food, functional cosmetics and sanitary products.

[0018] The above-mentioned application of isoflavone compounds, wherein the dosage form of the medicine and health food is at least one of injection, tablet, capsule, soft capsule, pill, granule, spray, aerosol, oral liquid, cream, gel, patch and inhalant.

[0019] The above-mentioned application of isoflavone compounds, wherein the type of the functional cosmetics includes at least one of lung protection spray, lung protection gel, lung protection mask and lung protection essence.

[0020] In the above-mentioned application of the isoflavone compound, the type of the sanitary product includes at least one of a dust mask, a protective mask, an air purification wipe and a medical gauze.

[0021] According to the results of animal experiments, this isoflavone compound can play a protective role in lung inflammation, fibrosis, and epithelial-mesenchymal transition caused by silica dust exposure in animal models, significantly reducing damage to lung tissue.

[0022] The isoflavone compound of the present invention is used in the preparation of a product for the prevention and / or treatment of silicosis. The compound protects lung tissue from damage caused by silica dust particles. At an effective dose of 25 mg / kg to 50 mg / kg, the compound significantly improves lung inflammation, fibrosis, decreased lung function, and immune dysfunction caused by silica dust exposure. BRIEF DESCRIPTION OF THE DRAWINGS

[0023] Figure 1HE staining of lung tissue of mice obtained in Example 1 of the present application, showing that three different doses of the compounds inhibited silica-induced lung inflammation in mice. The scale bar is 200 μm.

[0024] Figure 2 Masson staining pathological images of lung tissue obtained in Example 1 of the present application showing that three different doses of the compound inhibited silica-induced pulmonary fibrosis in mice. The scale bar is 200 μm.

[0025] Figure 3 This is an immunoblot image of the inhibition of silica-induced pulmonary fibrosis in mouse lung tissue by three different doses of the compound in Example 2 of the present application;

[0026] Figure 4 Fibronectin immunohistochemistry images of lung tissues of mice in Example 3 of the present application showing that three different doses of the compound inhibited silica-induced pulmonary fibrosis in mice. The scale bar is 200 μm.

[0027] Figure 5 The following are Col-III immunohistochemistry images of lung tissues of mice in Example 3 of the present application showing that three different doses of the compounds inhibited silica-induced pulmonary fibrosis in mice. The scale bar is 200 μm.

[0028] Figure 6 This is an immunohistochemical image of TGF-β1 in lung tissue of mice in Example 3 of the present application, showing that three different doses of the compound inhibited silica-induced pulmonary fibrosis in mice. The scale bar is 200 μm.

[0029] Figure 7 This is an immunoblot image of the inhibition of silica-induced epithelial-mesenchymal transition in mouse lung tissue by three different doses of compounds in Example 4 of the present application;

[0030] Figure 8 The immunohistochemical images of E-cadherin in lung tissue of mice in Example 5 are obtained by three different doses of the compound to inhibit silica-induced pulmonary fibrosis in mice. The scale bar is 200 μm.

[0031] Figure 9 Vimentin immunohistochemistry images of lung tissues of mice in Example 5, in which three different doses of the compounds inhibited silica-induced pulmonary fibrosis in mice. Scale bar: 200 μm.

[0032] Figure 10 This is a diagram showing the cytotoxicity test results of compound 1 in Example 6. DETAILED DESCRIPTION

[0033] In order to enable those skilled in the art to better understand the technical solution of the present invention, its specific implementation methods are described in detail below with reference to the accompanying drawings.

[0034] Application of isoflavone compounds in the preparation of products for preventing and / or treating silicosis, wherein the molecular formula of the isoflavone compounds is C 20 H 18 O5, the structural formula is shown in formula (1):

[0035]

[0036] In the following examples, compound 1 is used to refer to the isoflavone compound.

[0037] Example 1: Compound 1 alleviates silica-induced lung injury in mice

[0038] (1) Experimental methods:

[0039] Preparation of Compound 1: Dissolve Compound 1 in PBS containing 1% Tween-80 at a concentration of 5 mg / mL. Dissolve the positive drug pirfenidone in PBS containing 1% Tween-80 at a concentration of 40 mg / mL. The solvent is PBS containing 1% Tween-80.

[0040] The concentrations of the prepared solutions are 12.5 mg / kg, 25 mg / kg, and 50 mg / kg respectively.

[0041] Animal grouping: 30 6-8 week old C57BL / 6J male mice were divided into 6 groups with 5 mice in each group. The groups were normal group, model group, positive drug group, low-dose administration group, medium-dose administration group, and high-dose administration group.

[0042] Dosage and modeling: (1) Normal group: intratracheal instillation of 50 μL of normal saline; (2) Model group: intraperitoneal injection of solvent (10 mL / kg) 1 h before modeling. During modeling, the mice were fixed on the endotracheal intubation operating table at 60°. The mouse's mouth was gently opened and observed with a laryngoscope. The endotracheal intubation guide wire was inserted into the trachea, and 50 μL of SiO2 suspension (prepared with 10 ng / mL LPS, 0.1% Tween-80, and 2.5 mg / 25 μL SiO2) was instilled into the trachea. (3) Dosage group: intratracheal instillation of pirfenidone (200 mg / kg) or intraperitoneal injection of compound 1 (12.5 mg / kg, 25 mg / kg, 50 mg / kg) 1 h before modeling. The modeling steps were the same as above. Repeat every two days for 14 days.

[0043] Detection: 14 days after modeling, mice were euthanized and fixed on foam boards. Surgical scissors were used to dissect the mice along the midline of the abdomen. The skin was bluntly dissected, the thoracic cavity was opened, and the lung tissue was located and isolated. The lung tissue was washed with saline, dried, and stored in tissue fixative for HE staining, Masson staining, and immunohistochemical pathological examination. The alveolar wall, inflammatory cell infiltration, and collagen deposition in the lung tissue of the mice were observed.

[0044] (2) Experimental results:

[0045] See also Figure 1 and Figure 2 Compound 1, at three different concentrations, exhibited varying degrees of inhibitory effects on lung inflammation and fibrosis in mice. Compound 1 reversed the inflammatory cell infiltration and alveolar wall thickening caused by the inflammatory response in the lung tissue, resulting in improved alveolar wall integrity. It also reduced collagen deposition and Col-III protein levels in the lung tissue caused by fibrosis. This suggests that Compound 1 effectively ameliorates SiO2-induced lung inflammation and fibrosis in mice, demonstrating anti-inflammatory and anti-fibrotic effects in vivo.

[0046] Example 2: Immunoblotting detection of compound 1 inhibiting SiO2-induced pulmonary fibrosis protein expression in mice (1) Experimental method:

[0047] The preparation of compound 1 and solvent is the same as that in Example 1.

[0048] Animal grouping: Same as Example 1.

[0049] Administration and modeling: same as Example 1.

[0050] Testing: 14 days after modeling, mice were euthanized and fixed on foam boards. Surgical scissors were used to dissect the mice along the midline of the abdomen. The skin was bluntly dissected, the thoracic cavity was opened, and the lung tissue was located and isolated. The lung tissue was washed with saline, blotted dry, cut into small pieces, and stored in EP tubes at -80°C. The tissue was then homogenized, centrifuged, and lung protein was extracted. 6X Loading Buffer was added and the mixture was incubated in a boiling water bath for 5 minutes. SDS-PAGE electrophoresis was performed, and related proteins were detected by immunoblotting. The primary antibodies used were Fibronectin Polyclonal antibody (15613; Proteintech), Collagen Type III (N-terminal) Polyclonal antibody (22734; Proteintech), TGF Beta 1 Polyclonal antibody (21898; Proteintech), and Smooth Muscle actin Polyclonal antibody (14395; Proteintech). The internal control protein used was β-actin (66009-1; Proteintech).

[0051] (2) Experimental results:

[0052] See also Figure 3 Compound 1 at doses of 25 mg / kg and 50 mg / kg can reduce the levels of Fibronectin, Col-Ⅲ, and TGF-β1 proteins in the lung tissue of mice, indicating that compound 1 can effectively inhibit the expression of SiO2-induced lung fibrosis proteins, indicating that compound 1 has an anti-fibrotic effect in vivo.

[0053] Example 3: Immunohistochemical detection of compound 1 inhibiting SiO2-induced pulmonary fibrosis protein expression in mice

[0054] (1) Experimental methods:

[0055] The preparation of compound 1 and solvent is the same as that in Example 1.

[0056] Animal grouping: Same as Example 1.

[0057] Administration and modeling: same as Example 1.

[0058] Detection: 14 days after modeling, the mice were euthanized and fixed on a foam board. The mice were cut open along the midline of the abdomen with surgical scissors, the skin was bluntly separated, the chest cavity was opened, the lung tissue was found and separated. The lung tissue was washed with normal saline, the water was absorbed, cut into small pieces and divided into 4% paraformaldehyde for fixation for about 24 hours. The fixed lung tissue was dehydrated with gradient ethanol (70%, 85%, 95%, anhydrous ethanol) in sequence, each for 10 minutes. Treated with xylene twice for 10 minutes each, the tissue was immersed in melted paraffin, embedded to form paraffin blocks. The lung tissue was sliced ​​using a paraffin slicer with a thickness of 4-5μm. The slices were attached to anti-slip slides and baked in a 60°C oven for 1 hour to enhance adhesion. The slices were dewaxed by soaking in xylene twice for 10 minutes each. Hydrated with anhydrous ethanol, 95% ethanol, 85% ethanol, and 70% ethanol in sequence for 5 minutes each, and finally rinsed with distilled water. Incubate with trypsin (0.05%) at room temperature for 10-30 minutes, then wash with PBS. Incubate with 3% H2O2 solution at room temperature for 10 minutes to inhibit endogenous peroxidase activity. Block the sections with normal goat serum (1:10 dilution) or 5% BSA solution and incubate at room temperature for 30 minutes. Gently wash the sections with PBS for 3 times, 5 minutes each time. Place the sections in a humidified chamber, add the diluted primary antibody, and incubate overnight at 4°C. The primary antibodies used were Fibronectin Polyclonal antibody (15613; Proteintech), Collagen Type III (N-terminal) Polyclonal antibody (22734; Proteintech), and TGF Beta 1 Polyclonal antibody (21898; Proteintech). Add a secondary antibody labeled with horseradish peroxidase (HRP) (Goat Anti-Rabbit IgGHRP; A16104SAMPLE; Invitrogen) and dilute according to the manufacturer's instructions. Incubate at room temperature for 30-60 minutes, then wash three times with PBS for 5 minutes each. Use DAB (3,3'-diaminobenzidine) as a chromogenic substrate for 5-10 minutes. After color development, terminate the reaction with distilled water. Counterstain the cell nuclei with hematoxylin to develop a blue color. Counterstain for 30 seconds to 1 minute, then rinse with running water. Dehydrate with 70%, 85%, 95%, and anhydrous ethanol, sequentially for 5 minutes each. Treat with xylene twice for 10 minutes each. Mount the slides with neutral gum and cover with a coverslip. Finally, photograph under a microscope.

[0059] (2) Experimental results:

[0060] See also Figure 4 、 Figure 5 and Figure 6Compound 1 at doses of 25 mg / kg and 50 mg / kg can reduce the levels of Fibronectin, Col-Ⅲ, and TGF-β1 proteins in the lung tissue of mice, indicating that compound 1 can effectively inhibit the expression of SiO2-induced lung fibrosis proteins, indicating that compound 1 has an anti-fibrotic effect in vivo.

[0061] Example 4: Western blotting detection of compound 1 inhibiting SiO2-induced epithelial-mesenchymal transition protein expression in mouse lungs

[0062] (1) Experimental methods:

[0063] The preparation of compound 1 and solvent is the same as that in Example 1.

[0064] Animal grouping: Same as Example 1.

[0065] Administration and modeling: same as Example 1.

[0066] Detection: 14 days after modeling, mice were euthanized and fixed on foam boards. The mice were dissected open along the ventral midline using surgical scissors. The skin was bluntly dissected, the thoracic cavity was opened, and the lung tissue was located and isolated. The lung tissue was washed with saline, dried, cut into small pieces, and stored in EP tubes at -80°C. The tissue was then homogenized and centrifuged to extract lung tissue protein. 6X Loading Buffer was added and the mixture was in a boiling water bath for 5 minutes. SDS-PAGE electrophoresis was performed, and relevant proteins were detected by immunoblotting. The primary antibodies used were E-cadherin Polyclonal antibody (20874-1-AP; Proteintech) and Vimentin (N-terminal) Polyclonal antibody (10366-1-AP; Proteintech). The internal control protein used was β-actin (66009-1; Proteintech).

[0067] (2) Experimental results:

[0068] See also Figure 7 Compound 1 at doses of 25 mg / kg and 50 mg / kg increased E-cadherin protein expression in mouse lung tissue while decreasing Vimentin protein expression. This indicates that Compound 1 can effectively inhibit SiO2-induced EMT protein expression in lung tissue, demonstrating its anti-EMT activity in vivo.

[0069] Example 5: Immunohistochemical detection of compound 1 inhibiting SiO2-induced epithelial-mesenchymal transition protein expression in mouse lungs

[0070] (1) Experimental methods:

[0071] The preparation of compound 1 and solvent is the same as that in Example 1.

[0072] Animal grouping: Same as Example 1.

[0073] Administration and modeling: same as Example 1.

[0074] Detection: 14 days after modeling, the mice were euthanized and fixed on a foam board. The mice were cut open along the midline of the abdomen with surgical scissors, the skin was bluntly separated, the chest cavity was opened, the lung tissue was found and separated. The lung tissue was washed with normal saline, the water was absorbed, cut into small pieces and divided into 4% paraformaldehyde for fixation for about 24 hours. The fixed lung tissue was dehydrated with gradient ethanol (70%, 85%, 95%, anhydrous ethanol) in sequence, each for 10 minutes. Treated with xylene twice for 10 minutes each, the tissue was immersed in melted paraffin, embedded to form paraffin blocks. The lung tissue was sliced ​​using a paraffin slicer with a thickness of 4-5μm. The slices were attached to anti-slip slides and baked in a 60°C oven for 1 hour to enhance adhesion. The slices were dewaxed by soaking in xylene twice for 10 minutes each. Hydrated with anhydrous ethanol, 95% ethanol, 85% ethanol, and 70% ethanol in sequence for 5 minutes each, and finally rinsed with distilled water. Incubate with trypsin (0.05%) at room temperature for 10-30 minutes, then wash with PBS. Incubate with 3% H2O2 solution at room temperature for 10 minutes to inhibit endogenous peroxidase activity. Block the sections with normal goat serum (1:10 dilution) or 5% BSA solution and incubate at room temperature for 30 minutes. Gently wash the sections with PBS for 3 times, 5 minutes each time. Place the sections in a humidified chamber, add the diluted primary antibody, and incubate overnight at 4°C. The primary antibodies used were E-cadherin Polyclonal antibody (20874-1-AP; Proteintech) and Vimentin (N-terminal) Polyclonal antibody (10366-1-AP; Proteintech). Add a secondary antibody labeled with horseradish peroxidase (HRP) (Goat Anti-Rabbit IgG HRP; A16104SAMPLE; Invitrogen) and dilute according to the manufacturer's instructions. Incubate at room temperature for 30-60 minutes, then wash three times with PBS for 5 minutes each. Use DAB (3,3'-diaminobenzidine) as a chromogenic substrate for 5-10 minutes. After color development, terminate the reaction with distilled water. Counterstain the cell nuclei with hematoxylin to develop a blue color. Counterstain for 30 seconds to 1 minute, then rinse with running water. Dehydrate with 70%, 85%, 95%, and anhydrous ethanol, sequentially for 5 minutes each. Treat with xylene twice for 10 minutes each. Mount the slides with neutral gum and cover with a coverslip. Finally, photograph under a microscope.

[0075] (2) Experimental results:

[0076] See also Figure 8 and Figure 9 Compound 1 at doses of 5 mg / kg and 50 mg / kg increased E-cadherin protein expression in mouse lung tissue while decreasing Vimentin protein expression. This indicates that Compound 1 can effectively inhibit SiO2-induced EMT protein expression in lung tissue, demonstrating its anti-EMT activity in vivo.

[0077] Example 6: Cytotoxicity assay of compound 1

[0078] (1) Experimental methods:

[0079] When THP-1 cells reach the logarithmic phase of growth, it is most convenient to collect the cells, resuspend them, and seed them into 96-well plates at a density of 8,000 cells per well. Sterile PBS is added to the edge wells to prevent the cells from drying out. A control group, a negative group, and a drug concentration gradient group are set up. At the same time, 3-4 replicate wells are set up and the target concentration of the test compound is added to ensure that the final volume of each well is 100 μL. Place the cells in a constant temperature incubator for 24 hours to observe the cell state, and add 20 μL of MTT reagent at a concentration of 5 mg / mL to each well. Incubate in the constant temperature incubator for another 4 hours, discard the supernatant, add DMSO to each well, and shake on a shaker for 10 minutes to fully dissolve. Finally, the absorbance value of each well is measured on a microplate reader at a wavelength of 490 nm.

[0080] (2) Experimental results:

[0081] See also Figure 10 At a concentration of 200 μM, ZT-6 had no effect on THP-1 cells, and the cells showed good viability. It has a wide safety range and also exhibits no toxic side effects in animals.

[0082] In summary, the isoflavone compounds of the present invention protect lung tissue from damage caused by silica dust particles and can be used to prepare products for the prevention and / or treatment of silicosis. Furthermore, at an effective dose of 25 mg / kg to 50 mg / kg, the compounds can significantly improve lung inflammation, fibrosis, decreased lung function, and immune dysfunction caused by silica dust exposure.

[0083] Those skilled in the art should recognize that the above embodiments are merely intended to illustrate the present invention and are not intended to limit the present invention. As long as they are within the spirit of the present invention, any changes or modifications to the above embodiments will fall within the scope of the claims of the present invention.

Claims

1. Use of an isoflavone compound in the preparation of a product for preventing and / or treating silicosis, characterized in that: The molecular formula of the isoflavone compound is C 20 H 18 O5, the structural formula is shown in formula (1):

2. The use of the isoflavone compound according to claim 1, characterized in that The isoflavone compounds protect lung tissue from damage caused by silicosis by inhibiting the process of pulmonary fibrosis.

3. The use of the isoflavone compound according to claim 2, characterized in that: Pulmonary fibrosis is caused by fibroblast activation and excessive deposition of extracellular matrix.

4. The use of the isoflavone compound according to claim 1, characterized in that: The effective dosage of the isoflavone compound in the product for preventing and / or treating silicosis is 25 mg / kg to 50 mg / kg.

5. The use of the isoflavone compound according to claim 1, characterized in that: The isoflavone compound protects lung tissue from damage caused by silicosis by alleviating pulmonary fibrosis and inhibiting the epithelial-mesenchymal transition process.

6. The use of the isoflavone compound according to claim 1, characterized in that: The isoflavone compound reduces the toxic effect of silica dust particles on alveolar epithelial cells, inhibits the occurrence of epithelial-mesenchymal transition, and maintains the integrity of lung tissue structure and function.

7. The use of the isoflavone compound according to claim 1, characterized in that: The silicosis includes at least one of pulmonary fibrosis, respiratory dysfunction and related complications caused by long-term inhalation of silica dust.

8. The use of the isoflavone compound according to claim 1, characterized in that: The product includes at least one of medicines, health foods, functional cosmetics and sanitary products.

9. The use of the isoflavone compound according to claim 8, characterized in that: The dosage form of the medicine and health food is at least one of injection, tablet, capsule, soft capsule, granule, oral solution, pill, sustained-release tablet, film, ointment, cream, paste, gel, film coating, plaster and patch.

10. The use of the isoflavone compound according to claim 8, characterized in that: The types of the functional cosmetics include at least one of lung protection spray, lung protection gel, lung protection mask and lung protection essence.

11. The use of the isoflavone compound according to claim 8, characterized in that: The types of the sanitary products include at least one of dust masks, medical gauze, wet wipes and bandages.

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