Use of sesamin in preparation of products for improving and / or treating acute pancreatitis

Abstract

The application discloses application of sesamin in preparation of products for improving and / or treating acute pancreatitis and belongs to the technical field of biological pharmacy. The application provides application of sesamin in preparation of products for improving and / or treating acute pancreatitis. Sesamin has anti-inflammatory activity, can reduce the expression level of proinflammatory factors, reduce the content of serum amylase and lipase, reduce the expression level of M1 type macrophage related markers iNOS and CD86, and thus relieve the inflammatory reaction of acute pancreatitis. The results of examples show that sesamin has a definite therapeutic effect on acute pancreatitis by inhibiting M1 polarization of macrophages.

Description

Technical Field

[0001] This invention relates to the field of biopharmaceutical technology, and in particular to the use of sesamin in the preparation of products for improving and / or treating acute pancreatitis. Background Technology

[0002] Acute pancreatitis (AP) is an inflammatory response caused by the autodigestion of the pancreas by pancreatic enzymes. It is characterized by rapid onset, numerous complications, and high mortality, leading to pancreatic edema and necrosis. Severe AP can cause a series of peripancreatic complications and systemic inflammatory response syndrome, and in severe cases, organ failure and death. In this pathological process, the abnormal activation of pancreatic proteases secreted by the pancreas within pancreatic cells or the intercellular matrix, triggered by various etiologies, is a core initiating step. This abnormally activated proteases cause pancreatic cell damage, releasing damage-related molecular patterns, which in turn triggers the overactivation of the nuclear factor kappa B (NF-κB) inflammatory pathway. Activation of this pathway leads to the synthesis and secretion of large amounts of cytokines such as tumor necrosis factor, interleukin-1, and chemokines, inducing immune cells to aggregate towards the lesion to clear damaged tissue. However, when the inflammatory pathway is continuously overactivated, pro-inflammatory cytokines are released in a cascade amplification, resulting in the massive infiltration and abnormal activation of immune cells such as macrophages and neutrophils. This not only fails to repair the damage but also exacerbates pancreatic parenchymal destruction, ultimately inducing an uncontrollable systemic severe acute inflammatory response. Currently, Western medicine treatment for acute pancreatitis focuses on symptomatic relief and lacks specific drugs. Existing treatments (such as somatostatin and protease inhibitors) have limitations in their single mechanism of action and inability to halt the progression to severe illness. Commonly used symptomatic supportive measures (such as fluid resuscitation and blood purification) are costly, have limited plasma sources, and may cause disease transmission and allergic reactions. Traditional Chinese medicine plays an irreplaceable role in the treatment of acute and critical illnesses. The characteristics of Chinese medicine—multiple components, multiple targets, and multiple pathways of intervention—give it a unique advantage in the prevention and treatment of this disease. Meanwhile, basic research provides targets for the development of new drugs, but how to translate these findings into safe and effective clinical drugs remains a challenge.

[0003] Macrophages originate from monocytes and can polarize into different subtypes under the influence of various factors and environments. As an important component of the body's first line of defense in the immune system, they exhibit high cellular plasticity under physiological and pathological conditions. Therefore, precise regulation of macrophage activation is crucial for controlling disease progression and maintaining tissue homeostasis. M1 macrophages are mainly activated by lipopolysaccharide, producing large amounts of reactive oxygen species and pro-inflammatory cytokines, participating in the body's inflammatory response and tissue damage. Inflammation is the core mechanism for the occurrence and progression of acute pancreatitis.

[0004] Sesamin, a natural lignan compound, is widely found in various traditional Chinese medicine monomers. Sesamin is the most abundant lignan compound in sesame (CAS No.: 7076-24-6, molecular formula: C). 20 H 18 Sesamin (O6, molecular weight: 354.35) has been reported to have therapeutic effects on type 2 diabetic osteoporosis (T2DOP). Currently, there are no reports of using sesamin to treat acute pancreatitis. Summary of the Invention

[0005] The purpose of this invention is to provide the use of sesamin in the preparation of products for improving and / or treating acute pancreatitis, in order to solve the problems existing in the prior art.

[0006] To achieve the above objectives, the present invention provides the following solution: This invention provides the use of sesamin in the preparation of products for improving and / or treating acute pancreatitis.

[0007] This invention provides the use of sesamin in the preparation of products that inhibit M1 polarization of macrophages.

[0008] Optionally, the product may include a drug.

[0009] Optionally, the improvement and / or treatment of acute pancreatitis includes at least one of the following: 1) Reduce the expression levels of pro-inflammatory factors; 2) Reduce serum amylase and lipase levels; 3) Reduce the expression levels of immune inflammatory markers.

[0010] Optionally, the immune inflammatory markers include iNOS and / or CD86.

[0011] The present invention provides a product for improving and / or treating acute pancreatitis and inhibiting macrophage M1 polarization, the product comprising sesamin.

[0012] Optionally, the product may also include excipients; the excipients include any one or a combination of at least two of the following: carrier, diluent, excipient, filler, binder, wetting agent, disintegrant, emulsifier, cosolvent, solubilizer, osmotic pressure regulator, surfactant, coating material, colorant, pH adjuster, antioxidant, antibacterial agent, or buffer.

[0013] Optionally, the dosage form of the product may include granules, capsules, tablets, pills, or oral liquid.

[0014] This invention provides the application of sesamin in the preparation of S100 calcium-binding protein A9 inhibitor products. In the course of acute pancreatitis, macrophage M1 polarization is a key pathological process. Although S100A9 has been shown to participate in pancreatic damage caused by M1 polarization, research on traditional Chinese medicine monomers targeting S100A9 is still lacking. Sesamin inhibits M1 polarization by inhibiting S100A9, thereby improving acute pancreatitis. This invention fills this gap by providing the application of the traditional Chinese medicine monomer sesamin in the preparation of S100 calcium-binding protein A9 inhibitor products.

[0015] Optionally, the product may also include auxiliary materials.

[0016] Optionally, the excipients include any one or a combination of at least two of the following: carrier, diluent, excipient, filler, binder, wetting agent, disintegrant, emulsifier, cosolvent, solubilizer, osmotic pressure regulator, surfactant, coating material, colorant, pH adjuster, antioxidant, antibacterial agent, or buffer.

[0017] The present invention discloses the following technical effects: 1. This invention provides the use of sesamin in the preparation of products for improving and / or treating acute pancreatitis. The sesamin of this invention has anti-inflammatory activity, capable of reducing the expression levels of pro-inflammatory factors, reducing serum amylase and lipase levels, and reducing the expression levels of macrophage M1 polarization-related markers iNOS and CD86, thereby alleviating the inflammatory response.

[0018] 2. This invention provides the application of sesamin in the preparation of products that inhibit macrophage M1 polarization. The sesamin of this invention can significantly inhibit the release of lipopolysaccharide-induced inflammatory factors and reduce the expression of macrophage M1 polarization-related markers. Sesamin possesses pharmacological activities that inhibit excessive activation of inflammatory signaling pathways and downregulate the expression of pro-inflammatory factors; this characteristic is highly consistent with the key driving mechanism of macrophage M1 pro-inflammatory phenotype polarization in acute pancreatitis. Sesamin can block the amplification effect of the early inflammatory cascade in acute pancreatitis by intervening in the macrophage M1 polarization process. This invention screened and obtained sesamin, a traditional Chinese medicine monomer with anti-inflammatory activity. In vitro cell models were constructed for drug administration intervention, and the results confirmed that it can significantly inhibit cell M1 polarization. Based on this, in vivo animal experiments were conducted, and mice with acute pancreatitis were treated with 100 mg / kg sesamin, showing that it can effectively inhibit the pathological progression of acute pancreatitis.

[0019] 3. This invention provides the application of sesamin in the preparation of S100 calcium-binding protein A9 inhibitor products.

[0020] S100 calcium-binding protein A9 (S100 A9), also known as myeloid-related protein 14 (MRP14), is mainly expressed in myeloid cells and participates in the regulation of immune responses and inflammatory reactions. This protein is a key regulatory node in inflammatory signaling pathways, promoting M1 macrophage polarization and amplifying the cascade effect of pro-inflammatory cytokines. Existing studies have confirmed that S100A9 is significantly overexpressed in the pathological process of acute pancreatitis, and its expression level is positively correlated with disease severity and the intensity of systemic inflammatory response. Given the upstream regulatory role of S100A9 in the macrophage M1 polarization signal transduction process, targeting and inhibiting S100A9-mediated inflammatory pathway activation can provide a novel intervention direction for the clinical treatment of acute pancreatitis. This invention systematically elucidates the pharmacological effects of sesamin in improving acute pancreatitis from the perspective of S100A9 / M1 polarization regulation, which has important theoretical and practical value for revealing its molecular mechanism of action and expanding the application scope of clinical anti-inflammatory traditional Chinese medicine monomers. The purpose of this invention is to provide a novel application of sesamin, an active ingredient in traditional Chinese medicine, to inhibit macrophage M1 polarization and improve acute pancreatitis by targeting and inhibiting S100A9. This invention explores the role of sesamin in improving acute pancreatitis and verifies the anti-inflammatory activity of sesamin through in vitro and in vivo experiments, providing a theoretical basis for its efficacy verification. Attached Figure Description

[0021] To more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the drawings used in the embodiments will be briefly introduced below. Obviously, the drawings described below are only some embodiments of the present invention. For those skilled in the art, other drawings can be obtained based on these drawings without creative effort.

[0022] Figure 1 The graph shows the inhibitory effect of three traditional Chinese medicine monomers on S100A9 detected by an ELISA kit. Figure 2 The level of M1 polarized inflammatory factors was detected by qPCR in a RAW264.7 cell model. Figure 3 The graph shows the inhibitory effect of sesamin on M1 polarization in RAW264.7 cells. A represents the M1 polarization level detected by immunofluorescence in the RAW264.7 cell model, with a scale bar of 50µm per square. B is a statistical graph of the quantitative analysis results of the immunofluorescence experiment. C represents the M1 polarization level detected by flow cytometry in the RAW264.7 cell model. D is a statistical graph of the quantitative analysis results of the flow cytometry experiment. Figure 4 A graph showing the levels of M1 polarized inflammatory factors detected by qPCR in a BMDM cell model; Figure 5 This diagram illustrates the inhibitory effect of sesamin on M1 polarization in BMDM cells. A represents the M1 polarization level detected by immunofluorescence in the BMDM cell model, with a scale bar of 50µm per square. B is a statistical graph of the quantitative analysis results from the immunofluorescence experiment. C represents the M1 polarization level detected by flow cytometry in the BMDM cell model. D is a statistical graph of the quantitative analysis results from the flow cytometry experiment. Figure 6 The figures show the drug administration results in a mouse acute pancreatitis (AP) model. A is an HE staining image after drug administration in the AP model, with a scale bar of 100µm per square. B is a statistical graph of HE staining results. C shows the levels of inflammatory factors in the pancreas of AP mice detected by qPCR. D shows the serum lipase detection results in AP mice. E shows the serum amylase detection results in AP mice. Figures 1-6 In the diagram, ## represents the comparison between the M1 model group and the blank group. p <0.01; Compared to the M1 model group, the sesamin-treated group represents the difference between the two groups. p <0.05; Compared with the M1 model group, the sesamin-treated group represents the difference between the two groups. p <0.01. Detailed Implementation

[0023] Various exemplary embodiments of the present invention will now be described in detail. This detailed description should not be considered as a limitation of the present invention, but rather as a more detailed description of certain aspects, features, and embodiments of the present invention.

[0024] It should be understood that the terminology used in this invention is merely for describing particular embodiments and is not intended to limit the invention. Furthermore, with respect to numerical ranges in this invention, it should be understood that each intermediate value between the upper and lower limits of the range is also specifically disclosed. Any stated value or intermediate value within a stated range, as well as each smaller range between any other stated value or intermediate value within said range, is also included in this invention. The upper and lower limits of these smaller ranges may be independently included or excluded from the range.

[0025] Unless otherwise stated, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art. While only preferred methods and materials have been described herein, any methods and materials similar or equivalent to those described herein may be used in the implementation or testing of this invention. All references to this specification are incorporated by way of citation to disclose and describe methods and / or materials associated with those references. In the event of any conflict with any incorporated reference, the content of this specification shall prevail.

[0026] Various modifications and variations can be made to the specific embodiments described in this specification without departing from the scope or spirit of the invention, as will be apparent to those skilled in the art. Other embodiments derived from this specification will also be apparent to those skilled in the art. This specification and embodiments are merely exemplary.

[0027] The terms “include,” “including,” “have,” “contain,” etc., used in this article are all open-ended terms, meaning that they include but are not limited to.

[0028] Preparation of mouse bone marrow-derived macrophages: After sacrifice, C57 mice were disinfected by immersion in 75% alcohol for 5 minutes, the lower limb bones were aseptically separated, the muscles were dissected, the epiphyses were removed, and the bone marrow was washed with PBS to obtain cells; the cell suspension was filtered, centrifuged, and plated.

[0029] Example 1 (1) Experimental materials: Mouse S100 calcium binding protein A9 (S100A9) ELISA kit (Shanghai Langdun Biotechnology Co., Ltd. BPE20935), BMDM (mouse bone marrow-derived macrophages), 10% FBS medium, lipopolysaccharide LPS (Dalian Meilun Biotechnology MB5198), anti-inflammatory Chinese medicine active ingredient standard sesamin (99.6% sesamin content) (Yuanye Biotechnology A10331), Linarin (Dalian Meilun Biotechnology MB6786-1), and Wighteone (TargetMol TN5254), mouse macrophage colony-stimulating factor (Dalian Meilun Biotechnology MA0604).

[0030] (2) Experimental methods: After the C57 mice were sacrificed, they were disinfected by soaking in 75% alcohol for 5 min. The lower limb bones were aseptically separated, the muscles were dissected, the epiphyses were removed, and the bone marrow was washed with PBS to obtain cells. The cell suspension was filtered, centrifuged, and plated. The cells were cultured in DMEM high glucose medium containing 10% fetal bovine serum (FBS), 100 U / mL penicillin, 100 μg / mL streptomycin, 0.25 μg / mL amphotericin B and 20 ng / mL mouse macrophage colony-stimulating factor. The cells were cultured in an incubator for one week, and the medium was changed on the third day. After that, the cells were treated with drugs.

[0031] The experiment was conducted in the following groups: a blank control group, an M1 model group, and a drug-treated group. The blank control group received no inflammatory stimulation or drug treatment. The M1 model group was stimulated with lipopolysaccharide (LPS, 1 μg / mL) for 24 h to induce the formation of the M1 pro-inflammatory phenotype in BMDM. The drug-treated groups received LPS stimulation along with corresponding traditional Chinese medicine monomer standards (Mongolian glycoside, sesamin, and white ketone, 10 μM) for 24 h. After 24 h, the supernatant was collected, and the inhibitory effect on S100A9 was detected using an ELISA kit.

[0032] Data processing: The results of the ELISA kit detection by the microplate reader were analyzed and statistically analyzed, and a bar chart was plotted.

[0033] (3) Results and Analysis: When administered in the M1 state of BMDM, the reagent kit showed that sesamin had the best inhibitory effect on S100A9, see [link to kit]. Figure 1 It can be seen that sesamin has a good inhibitory effect on S100A9.

[0034] Example 2: Sesamin's efficacy in inhibiting M1 polarization in RAW264.7 and BMDM cells. (1) Experimental materials: RAW264.7 mouse macrophage cell line (ATCC), BMDM (mouse bone marrow-derived macrophages), 10% FBS DMEM high glucose medium, lipopolysaccharide LPS, sesamin, etc.

[0035] (2) Experimental method: After the RAW264.7 cells were revived, they were cultured in DMEM high glucose medium containing 10% fetal bovine serum (FBS) at 37°C and 5% CO2 in a humid atmosphere. After the cells adhered to the wall, they were treated with drugs.

[0036] (3) BMDM (mice bone marrow-derived macrophages): After C57 mice were sacrificed, they were disinfected by soaking in 75% alcohol for 5 min, the lower limb bones were aseptically separated, the muscles were dissected, the epiphyses were removed, and the bone marrow was washed with PBS to obtain cells; the cell suspension was filtered, centrifuged and plated, and cultured in DMEM high glycosyl containing 10% fetal bovine serum (FBS), penicillin 100 U / mL, streptomycin 100 μg / mL, amphotericin B 0.25 μg / mL and mouse macrophage colony-stimulating factor 20 ng / mL. The cells were cultured in an incubator for one week, and the cell medium was changed on the third day of culture. After that, the cells were grouped and treated with drugs.

[0037] The experiment was conducted in the following groups: blank control group, M1 model group, and sesamin treatment group. The blank control group received no inflammatory stimulation or drug treatment. The M1 model group was stimulated with lipopolysaccharide (LPS, 1 μg / mL) for 24 h to induce the formation of the M1 pro-inflammatory phenotype in RAW264.7 and BMDM cells. The treatment groups received LPS stimulation along with the corresponding Chinese herbal monomer standard sesamin (10 μM) for 24 h. After 24 h, cells were collected for qPCR, immunofluorescence, and flow cytometry to detect the inhibitory effect of drug treatment on macrophage M1 polarization.

[0038] Data processing: The results of qPCR and flow cytometry experiments were analyzed and statistically analyzed, and bar charts were plotted. Three images were randomly selected from each group of immunofluorescence results for quantitative analysis. The results were then analyzed and statistically analyzed, and bar charts were plotted.

[0039] (4) Results and Analysis: qPCR results showed that IL-1β, IL-6, Tnf-α, and other indicators were significantly increased in the M1 model group. Compared with the M1 model group, the mRNA expression levels of related indicators IL-1β, IL-6, Tnf-α, iNOS, and CD86 in the sesamin-treated group were significantly decreased, indicating that sesamin treatment could inhibit macrophage M1 polarization. Figure 2 , Figure 4 ).

[0040] Immunofluorescence assays showed that the iNOS fluorescence intensity was significantly enhanced in the LPS-induced M1 model group, while the iNOS fluorescence intensity was significantly reduced in the sesamin-treated group compared to the M1 model group. Figure 3 China A Figure 5 (A) This suggests that treatment with sesamin can reduce the M1-type inflammatory phenotype in cells. iNOS (inducible nitric oxide synthase) is a classic pro-inflammatory marker of M1-type macrophages; increased fluorescence intensity usually reflects elevated intracellular iNOS protein expression levels, indicating enhanced macrophage pro-inflammatory phenotype. The above results indicate that sesamin can reduce iNOS expression levels, regulate the M1-type inflammatory phenotype in cells, and thus exert an anti-inflammatory effect.

[0041] To further quantify the immunofluorescence results, the changes in intracellular iNOS protein expression levels were evaluated by calculating the mean fluorescence intensity (MFI). The results showed that LPS stimulation significantly increased the mean fluorescence intensity of iNOS in cells, while sesamin intervention significantly decreased the mean fluorescence intensity of iNOS. Figure 3 B, Figure 5 (B) indicates that sesamin can reduce LPS-induced iNOS expression levels.

[0042] Figure 3 and Figure 5 In this study, DAPI was used for nuclear localization, F4 / 80 for macrophage identification, iNOS for evaluating the M1 inflammatory phenotype, and Merge for observing the co-localization of iNOS and the macrophage marker F4 / 80. The results further demonstrate that sesamin can reduce iNOS expression in macrophages and inhibit the M1 inflammatory phenotype.

[0043] Flow cytometry results showed that the proportion of M1 polarization in cells of the M1 model group was significantly increased, while the proportion of M1 polarization in cells of the sesamin-treated group was significantly decreased, indicating that the drug administration could inhibit macrophage M1 polarization. Figure 3 C, Figure 5 (C)

[0044] To further quantify the M1 polarization level of macrophages, the proportion of iNOS-positive cells in the F4 / 80-positive macrophage population was detected by flow cytometry. + / iNOS + The proportion of double-positive cells is defined as the M1 polarization ratio (%). The M1 polarization ratio reflects the change in the proportion of M1 pro-inflammatory phenotype cells in the total macrophage population. Figure 3 D, Figure 5 (D), LPS stimulation significantly increased the M1 polarization ratio, while sesamin intervention significantly decreased the M1 polarization ratio, indicating that sesamin can reduce the M1 polarization level of macrophages.

[0045] Example 3: Efficacy Experiment of Sesamin in the Treatment of Acute Pancreatitis (1) Experimental materials: taurine, sesamin, physiological saline, gavage needle, 1 mL syringe, etc.

[0046] (2) Experimental methods: 4-6 week old C57BL / 6J mice were randomly divided into 3 groups: normal group, model group, and sesamin administration group, with 6 mice in each group, for a total of 18 mice. The model group and the administration group mice were used to establish an acute pancreatitis (AP) model by intraperitoneal injection of lipolytic acid (LPS).

[0047] Model group (AP): 10 injections of hymenoplasmin were given in one day, each injection was 100 μg / kg, with an interval of 1 hour between each injection. After the last injection of hymenoplasmin, an injection of LPS was given, with an LPS injection dose of 10 mg / kg.

[0048] Sesamin administration group: Sesamin was injected 10 times a day, with each injection being 100 μg / kg, with each injection spaced 1 hour apart. After the last injection of sesamin, LPS was injected at a dose of 10 mg / kg. Sesamin (100 mg / kg) was administered by gavage 12 hours after the first injection of sesamin.

[0049] Normal group (Ctrl): Administered an equal volume of normal saline throughout the entire process (by injection and gavage).

[0050] The day after the experimental model was established, mice were euthanized and blood and pancreatic tissue were collected. A portion of the pancreatic tissue was fixed in a tissue fixative for pathological staining; another portion was cryopreserved at -80°C for qPCR and other detections. Serum was separated from the mouse blood and cryopreserved at -80°C for the detection of lipase, amylase, etc.

[0051] Data processing: Pancreatic tissue was stained with hematoxylin and eosin (HE). Three stained images were randomly selected from each group for pathological scoring. The results were statistically analyzed and plotted as bar charts. qPCR analysis was performed on M1-related indicators (IL-1β, IL-6, Tnf-α). The results of amylase and lipase assays obtained using an ELISA reader were analyzed, statistically analyzed, and plotted as bar charts.

[0052] Results and Analysis: HE staining results showed ( Figure 6 In mice in groups A and B, the pancreatic tissue of the model group showed obvious necrosis, edema, and inflammatory infiltration. Compared with the model group, the degree of the above pathological changes in the pancreas of mice in the sesamin-treated group was significantly reduced, indicating that sesamin has a clear therapeutic effect on acute pancreatitis.

[0053] qPCR results showed ( Figure 6 In the acute pancreatitis model group (AP model group), the mRNA expression levels of pro-inflammatory factors IL-1β, IL-6, TNF-α, and M1 macrophage-related markers iNOS and CD86 in the pancreatic tissue of mice were significantly increased. Compared with the acute pancreatitis model group, the expression levels of the above-mentioned inflammatory markers in the pancreatic tissue of mice in the sesamin administration group were significantly decreased, suggesting that sesamin can reduce the inflammatory response during acute pancreatitis and regulate the M1 macrophage-related inflammatory phenotype, thereby playing a role in improving acute pancreatitis.

[0054] Results of lipase and amylase ( Figure 6(D and E): The levels of lipase and amylase in the serum of mice in the model group were significantly increased, while the levels of lipase and amylase in the serum of mice in the sesamin-treated group were significantly decreased, indicating that sesamin administration can reduce their levels and thus alleviate acute pancreatitis.

[0055] The embodiments described above are merely preferred embodiments of the present invention and are not intended to limit the scope of the present invention. Various modifications and improvements made by those skilled in the art to the technical solutions of the present invention without departing from the spirit of the present invention should fall within the protection scope defined by the claims of the present invention.

Claims

1. The use of sesamin in the preparation of products for improving and / or treating acute pancreatitis.

2. Application of sesamin in the preparation of products that inhibit macrophage M1 polarization.

3. The application according to claim 1 or 2, characterized in that, The products include pharmaceuticals.

4. The application according to claim 1, characterized in that, The improvement and / or treatment of acute pancreatitis includes at least one of the following: 1) Reduce the expression levels of pro-inflammatory factors; 2) Reduce serum amylase and / or lipase levels; 3) Reduce the expression levels of immune inflammatory markers.

5. A product for improving and / or treating acute pancreatitis and inhibiting macrophage M1 polarization, characterized in that, The product includes sesamin.

6. The product according to claim 5, characterized in that, The product also includes excipients; the excipients include any one or a combination of at least two of the following: carrier, diluent, excipient, filler, binder, wetting agent, disintegrant, emulsifier, cosolvent, solubilizer, osmotic pressure regulator, surfactant, coating material, colorant, pH adjuster, antioxidant, antibacterial agent or buffer.

7. The product according to claim 5, characterized in that, The dosage forms of the product include granules, capsules, tablets, pills, or oral liquids.

8. Application of sesamin in the preparation of S100 calcium-binding protein A9 inhibitor products.

9. The application according to claim 8, characterized in that, The product also includes auxiliary materials.

10. The application according to claim 9, characterized in that, The excipients include any one or a combination of at least two of the following: carrier, diluent, excipient, filler, binder, wetting agent, disintegrant, emulsifier, cosolvent, solubilizer, osmotic pressure regulator, surfactant, coating material, colorant, pH adjuster, antioxidant, antibacterial agent, or buffer.

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