Application of flavonoids in bidentate in preparation of blood sugar reducing medicine or functional food

Abstract

The application belongs to the technical field of medicine or health food, and particularly relates to application of 5-hydroxy-6,7-dimethoxylflavone in preparation of blood sugar reducing medicine or functional food. The application finds a new use of 5-hydroxy-6,7-dimethoxylflavone through a large number of researches and tests, and 5-hydroxy-6,7-dimethoxylflavone has a remarkable blood sugar reducing effect, can promote islet beta cell regeneration, and promote islet alpha cell transdifferentiation to beta cell. Therefore, 5-hydroxy-6,7-dimethoxylflavone can be used to prepare medicine for promoting islet beta cell regeneration and promoting islet alpha cell transdifferentiation to beta cell. Thus, 5-hydroxy-6,7-dimethoxylflavone can be used to prepare blood sugar reducing medicine or functional food, including medicine for preventing and radically treating diabetes or functional food for assisting high blood sugar or diabetes in reducing blood sugar.

Description

Technical Field

[0001] This invention belongs to the field of pharmaceutical or health food technology, specifically relating to the application of 5-Hydroxy-6,7-dimethoxylflavone in the preparation of hypoglycemic drugs or functional foods. Background Technology

[0002] Diabetes is a common metabolic disease worldwide. During its progression, it is mainly caused by a decrease in the number and loss of function of pancreatic beta cells that secrete insulin, which seriously deteriorates people's health and quality of life.

[0003] Current treatment options include oral hypoglycemic agents or insulin injections, which can temporarily control blood sugar levels; however, these therapies do not prevent diabetic complications and are associated with adverse reactions such as hypoglycemia. Currently, the global scientific research community has introduced many new diabetes treatments, and replacing missing insulin-secreting cells may restore normal insulin secretion and cure patients. However, while there are successful clinical cases of islet cell transplantation, suitable islets for transplantation are usually obtained from brain-dead donors, making the number of available donors very limited. Furthermore, to prevent rejection, patients need to take immunosuppressive drugs long-term, which not only increases the risk of complications but may also affect the function of other organs. Of particular interest is transdifferentiation cell therapy, a novel approach based on the above global developments, which may lead to breakthroughs in the treatment of diabetes in the future. Starting with islet cells, transdifferentiating other redundant endocrine cells in the patient into insulin-producing islet beta cells has the potential to move from treating the symptoms to curing the root cause of diabetes. This method can effectively increase the number of beta cells, thereby improving insulin secretion and helping to control blood sugar levels. This method utilizes existing cellular resources within the body, avoiding the need for exogenous islet transplantation and thus reducing the risks of donor shortages and immune rejection. It offers a new treatment approach for diabetic patients. This method not only has potential clinical application value but also contributes to a deeper understanding of the plasticity and regeneration mechanisms of pancreatic cells, thereby advancing the development of diabetes treatment. Summary of the Invention

[0004] The purpose of this invention is to provide the application of flavonoids in the preparation of hypoglycemic drugs.

[0005] To overcome the shortcomings of the prior art, the present invention provides the following technical solution: Applications of flavonoids in the preparation of hypoglycemic drugs, drugs for the prevention or treatment of diabetes, or functional foods that help lower blood sugar in patients with hyperglycemia or diabetes.

[0006] Furthermore, the flavonoids from the senna promote the regeneration of pancreatic beta cells.

[0007] Furthermore, the flavonoids from the senna promote the transdifferentiation of pancreatic alpha cells into beta cells.

[0008] Furthermore, the diabetes includes type 1 diabetes, type 2 diabetes, gestational diabetes, or special types of diabetes.

[0009] Furthermore, the flavonoids from the purslane act on the Pdx1 gene, enhancing the function of pancreatic beta cells.

[0010] Compared with the prior art, the technical solution of the present invention has at least the following technical effects: This invention, through extensive research and experimentation, has discovered a novel use for purslane flavonoids, demonstrating a significant effect in lowering blood sugar. It promotes the regeneration of pancreatic beta cells and the transdifferentiation of pancreatic alpha cells into beta cells. Therefore, purslane flavonoids can be used to prepare drugs and functional foods that promote the regeneration of pancreatic beta cells and the transdifferentiation of pancreatic alpha cells into beta cells. Consequently, purslane flavonoids can be used to prepare hypoglycemic drugs or functional foods, including drugs for the prevention and treatment of diabetes or functional foods that assist in lowering blood sugar in patients with hyperglycemia or diabetes. Attached Figure Description

[0011] The accompanying drawings, which form part of this application, are used to provide a further understanding of the invention. The illustrative embodiments of the invention and their descriptions are used to explain the invention and do not constitute an undue limitation of the invention. Wherein: Figure 1 The images show fluorescence imaging of pancreatic beta cell proliferation promoted by flavonoids in Example 1, as well as a statistical diagram of beta cell count.

[0012] Figure 2 This is a cell fluorescence imaging image showing how flavonoids from *Capsella bursa-pastoris* promote the transdifferentiation of pancreatic alpha cells into beta cells in Example 2. Figure 3 The bar chart shows the number of pancreatic alpha cells that underwent transdifferentiation into beta cells promoted by tataric acid flavonoids in Example 2. Figure 4 This is a bar chart showing the hypoglycemic effect of tataric acid flavonoids in a diabetic zebrafish model in Example 3.

[0013] Figure 5 This is a bar chart showing the effect of flavonoids from *Tamarix chinensis* on the expression of the Pdx1 gene in the alpha cell line in Example 4.

[0014] In the attached image, "mcherry" +"cell number" indicates the number of mcherry-positive cells; "eGFP cell number" indicates the number of eGFP-positive cells; "Glucose / larvae" indicates the glucose content or concentration in each zebrafish larvae; "Pdx1 Relative luciferase activity" indicates the relative luciferase activity of Pdx1.

[0015] Terminology Explanation Unless otherwise stated, all technical terms used in this invention have the same meaning as commonly understood by one of ordinary skill in the art. All patents and publications related to this invention are incorporated herein by reference in their entirety.

[0016] The technical terms involved in this invention are explained as follows: The term "pancreatic beta cells" refers to a type of islet cell located primarily in the islets of Langerhans within the pancreas. Their main function is to synthesize and secrete insulin. When the body eats, blood sugar levels rise, and pancreatic beta cells sense this change and release insulin. Insulin prompts cells to take up and utilize glucose, thereby lowering blood sugar levels.

[0017] The term "alpha cell" refers to another important cell type in the pancreas, responsible for secreting glucagon, which is the opposite of the function of beta cells. When the body is in a state of low blood sugar, such as fasting or during exercise, alpha cells secrete glucagon. Glucagon promotes glycogenolysis and gluconeogenesis, raising blood sugar levels. For example, when a person has not eaten for a long time, alpha cells release glucagon to prevent hypoglycemia and ensure energy supply to vital organs.

[0018] The term "pancreatic beta cells" refers to a type of pancreatic cell primarily located within the islets of Langerhans. These are key cells in regulating blood sugar levels, sensing changes in blood glucose concentration. When blood sugar rises, pancreatic beta cells synthesize and secrete insulin. Insulin prompts cells to take up and utilize glucose, promotes glycogen synthesis, and inhibits gluconeogenesis, thereby lowering blood sugar levels. For example, after eating, when blood sugar rises, pancreatic beta cells release insulin to maintain blood sugar within a normal range. If pancreatic beta cells are damaged, resulting in insufficient or abnormal insulin secretion, diabetes may develop.

[0019] The term "type 1 diabetes" is an autoimmune disease caused by the destruction of pancreatic beta cells by the patient's own immune system, resulting in an absolute deficiency of insulin secretion. Patients need to rely on insulin treatment for life and must supplement insulin from external sources.

[0020] The term "type 2 diabetes" refers to insulin resistance and a relative deficiency of insulin. Insulin resistance means that cells are "insensitive" to insulin, which cannot work effectively, thus leading to elevated blood sugar levels.

[0021] The term "Pdx1 gene" stands for Pancreatic and Duodenal Homeobox-1, a gene that plays a crucial role in the development of an organism. It is primarily involved in pancreatic development, including the formation of islet cells and acinar cells. In adults, the Pdx1 gene regulates the function of pancreatic beta cells, maintaining their normal insulin secretion activity. For example, abnormal expression of the Pdx1 gene may lead to pancreatic hypoplasia or pancreatic beta cell dysfunction, which is closely related to the development of diabetes.

[0022] The term "prevention" refers to avoiding or reducing the risk of infection, experiencing, suffering from, or having a disease, condition, ailment, injury, or health problem, or avoiding or reducing the development or progression of such a state and / or its symptoms. As used herein, the term "prevention" refers to reducing the risk of developing diabetes by taking medications that lower blood sugar.

[0023] The term "treatment" refers to reducing or eliminating the cause and / or effects or symptoms of a condition or disease. As used in this article, "treatment" refers to controlling blood sugar levels, delaying the onset and progression of complications, and maintaining indicators such as blood glucose and glycated hemoglobin within a reasonable range by taking blood glucose-lowering medications.

[0024] According to a first aspect of the present invention, the use of 5-Hydroxy-6,7-dimethoxylflavone in the preparation of hypoglycemic drugs, drugs for the prevention or treatment of diabetes, or functional foods that assist in lowering blood sugar in patients with hyperglycemia or diabetes is provided. 5-Hydroxy-6,7-dimethoxylflavone, also known as Mosloflavone, has the following structure: Its CAS number is 740-33-0, and its molecular formula is C. 17 H 14 O5 has a molecular weight of 298.294.

[0025] In the above-mentioned application of flavonoids in the preparation of hypoglycemic drugs, as a preferred embodiment, it enhances the function of pancreatic islet beta cells and promotes the regeneration of pancreatic islet beta cells, specifically involving promoting the transdifferentiation of pancreatic islet alpha cells into beta cells and increasing the number and function of pancreatic islet beta cells.

[0026] The innovative mechanism of action of flavonoids from purslane on pancreatic islet cell transdifferentiation provided by this invention includes a unique target on pancreatic islet cells. It emphasizes that the compound acts on the Pdx1 gene, thereby enhancing the function of pancreatic beta cells, promoting insulin secretion, and achieving transdifferentiation.

[0027] In the above-mentioned application of tataric acid flavonoids in the preparation of hypoglycemic drugs, as a preferred embodiment, diabetes includes type 1 (insulin-dependent) diabetes, type 2 (non-insulin-dependent) diabetes, gestational diabetes, or special types of diabetes.

[0028] In the above-mentioned application of purslane flavonoids in the preparation of hypoglycemic drugs, as a preferred embodiment, the purslane flavonoids act on the Pdx1 gene to enhance the function of pancreatic beta cells.

[0029] The hypoglycemic drugs of the present invention are suitable for oral administration in the following forms: tablets (uncoated or coated tablets, such as those having an anti-gastric acid or delayed-dissolution or insoluble coating that controls the release of the compounds of the present invention), tablets or films / rice paper capsules that disintegrate rapidly in the oral cavity, films / lyophilized forms or capsules (e.g., hard or soft gelatin capsules), sugar-coated tablets, granules, pills, powders, emulsions, suspensions, aerosols or solutions. Detailed Implementation

[0030] To make the objectives, technical solutions, and advantages of this invention clearer, the technical solutions in the embodiments of this invention will be clearly and completely described below in conjunction with the embodiments of this invention. Those skilled in the art should understand that the embodiments described are merely illustrative of the invention and should not be considered as specific limitations thereof. All other embodiments obtained by those skilled in the art based on the embodiments of this invention without creative effort are within the scope of protection of this invention. Process parameters not specifically specified in the following embodiments are generally performed under conventional conditions.

[0031] The endpoints and any values ​​of the ranges disclosed in this invention are not limited to the precise ranges or values, and these ranges or values ​​should be understood to include values ​​close to these ranges or values. For numerical ranges, the endpoint values ​​of the various ranges, the endpoint values ​​of the various ranges and individual point values, and individual point values ​​can be combined with each other to obtain one or more new numerical ranges, which should be considered as specifically disclosed in this invention.

[0032] It should be further appreciated that certain features of the invention, for clarity, have been described in multiple independent embodiments, but may also be provided in combination in a single embodiment. Conversely, various features of the invention, for brevity, have been described in a single embodiment, but may also be provided individually or in any suitable sub-combination.

[0033] The present invention will now be described in detail with reference to embodiments thereof. These examples are provided by way of explanation and not by way of limitation. In fact, those skilled in the art will recognize that modifications and variations can be made to the present invention without departing from its scope or spirit. For example, a feature shown or described as part of one embodiment may be used in another embodiment to produce yet another embodiment. Therefore, it is desirable that the present invention encompass such modifications and variations that fall within the scope of the appended claims and their equivalents.

[0034] In the embodiments of the present invention, unless otherwise specified, the experimental methods used are conventional methods, and the materials and reagents used are commercially available unless otherwise specified.

[0035] “dpf” indicates the number of days past fertilization.

[0036] "Final concentration" refers to the concentration of a drug or other reagent in the entire culture medium system after it has been added to the culture medium.

[0037] The composition of 30× Daniel Buffer is shown in Table 1 (the 0.3× Daniel Buffer used in the embodiments of the present invention is 30× Daniel Buffer dissolved in water): Table 1 To prepare a 0.3× Daniel Buffer: Dilute a 30× Daniel Buffer with water by 100 times to obtain a 0.3× Daniel Buffer.

[0038] DMSO stands for dimethyl sulfoxide.

[0039] Tg(Ins:htBidTE-ON;LR) Transgenic zebrafish: from Wenbiao Chen's laboratory at Vanderbilt University.

[0040] Tg(Ins:H2BmCherry) genetically modified zebrafish: from Wenbiao Chen's laboratory at Vanderbilt University.

[0041] Tg(arx:Cre) transgenic zebrafish: from Didier Stainier's laboratory at the Max Planck Institute in Germany.

[0042] Tg(ins:loxP:mCherrySTOP:loxP:H2B-eGFP) transgenic zebrafish: from Didier Stainier's laboratory at the Max Planck Institute in Germany.

[0043] Example 1: 5-Hydroxy-6,7-dimethoxylflavone promotes the regeneration of beta cells in Tg(Ins:htBidTE-ON;LR) and Tg(Ins:H2BmCherry) transgenic zebrafish. (a) Transgenic zebrafish of Tg(Ins:htBidTE-ON;LR) and Tg(Ins:H2BmCherry) were mated. In Tg(Ins:htBidTE-ON;LR) transgenic zebrafish, the expression of the pro-apoptotic protein truncated as Bid (tBid) under the insulin-labeled beta cell promoter (Ins) was controlled by two compounds, doxycycline and tebufenozide. The addition of these two compounds induced tBid expression, leading to beta cell apoptosis. Based on this, a diabetic zebrafish model of beta cell ablation was established. Tg(Ins:H2BmCherry) indicates that beta cells were labeled as mCherry-positive red cells for beta cell counting.

[0044] Newly hatched zebrafish eggs were placed in 0.3× Daniel Buffer and cultured in a light incubator. The conditions of the light incubator were: a light-to-dark time ratio of 14:10 and a temperature of 28.5℃.

[0045] (ii) Drug induction: Add 6 ml of 0.3×Daniel Buffer to a 6 cm culture dish. Transfer zebrafish eggs (2 dpf, source and culture conditions see step (I) of Example 1) to the culture dish, add 3 μL of 50 mM doxycycline and 3 μL of 25 mM tebufenozide, and gently shake the culture dish to mix. Then wrap it with aluminum foil to protect it from light and place it in a light incubator for 48 h.

[0046] (III) Chemical Dosing Treatment: Rinse the zebrafish larvae with fresh culture medium to remove any residual inducers (doxycycline and tebufenozide), then transfer them to fresh culture medium. Add 1 ml of zebrafish embryo culture medium to each well of a 24-well plate, followed by 1 ml of 0.3×Daniel Buffer. Then add 1 μl of a 2.5 mM solution of citrinum flavonoids (dissolved in DMSO), and incubate for 24 h under light. The control group was treated with 1 μl of DMSO under the same culture conditions and is designated as the Control group.

[0047] (iv) Fixation of zebrafish: The drug-treated zebrafish juveniles were transferred to 1.5 mL centrifuge tubes and then fixed with 4% paraformaldehyde; the fixation conditions were 4°C and overnight.

[0048] (v) Counting of mCherry-positive cells in zebrafish: Zebrafish juveniles were transferred to a glass slide with their right side facing up. A 10 μL mounting medium was then added to the slide for mounting. After mounting, the number of cells exhibiting red fluorescence (representing beta cells) was counted under a fluorescence microscope. The experimental results are as follows: Figure 1 As shown. Among them, Figure 1 This image shows a fluorescence imaging study of pancreatic islet beta cell proliferation promoted by purslane flavonoids in this embodiment, along with a statistical graph of the number of beta cells. The image shows that purslane flavonoid treatment can increase the number of beta cells in a diabetic zebrafish model, demonstrating an effect on restoring pancreatic islet beta cell regeneration.

[0049] Example 2: 5-Hydroxy-6,7-dimethoxylflavone promotes the transdifferentiation of pancreatic alpha cells into beta cells. (a) Two transgenic zebrafish, Tg(arx:Cre) and Tg(ins:loxP:mCherrySTOP:loxP:H2B-eGFP), were mated to obtain zebrafish eggs. The resulting zebrafish eggs simultaneously possessed transgenes of both Tg(arx:Cre) and Tg(ins:loxP:mCherrySTOP:loxP:H2B-eGFP), meaning they contained the insulin promoter, the mcherry-stop fragment, the H2BeGFP gene, Arx, and Cre genes. Downstream of the insulin promoter in the zebrafish eggs was a mcherry-stop fragment containing a LoxP site and the H2BeGFP gene. In the presence of Cre recombinase driven by the Arx (alpha cell characteristic transcription factor) promoter, Cre-mediated recombination occurred, cleaving the mcherry-stop fragment and enabling the insulin promoter to drive H2BeGFP gene expression. Therefore, the expression of the green fluorescent protein eGFP could be used to determine whether alpha cells had transdifferentiated into beta cells.

[0050] Newly hatched zebrafish eggs from mating two transgenic zebrafish species, Tg(arx:Cre) and Tg(ins:loxP:mCherrySTOP:loxP:H2B-eGFP), were cultured in 0.3×Daniel Buffer in a light incubator. The conditions of the light incubator were: a light-to-dark time ratio of 14:10 and a temperature of 28.5℃.

[0051] (II) Drug treatment: Zebrafish juveniles (5 dpf, source and culture conditions are described in step (I) of Example 2) were transferred to 24-well plates. 1 ml of zebrafish embryo culture medium was added to each well, and 1 μl of 2.5 mM senna flavonoid solution (dissolved in DMSO) was added to each well. The plates were then treated in a light incubator for 24 hours to obtain the senna flavonoid group.

[0052] The control group was treated with 1 μl of DMSO under the same culture conditions and in a light incubator for 24 hours. This group was designated as the Control Group.

[0053] (III) Fixation of Zebrafish: The drug-treated zebrafish juveniles were transferred to 1.5 mL centrifuge tubes and then fixed with 4% paraformaldehyde; the fixation conditions were 4°C and overnight.

[0054] (iv) Counting of zebrafish eGFP-positive cells: The zebrafish juveniles were transferred to a glass slide with their right side facing up. 10 μL of mounting medium was dropped onto the slide for mounting. After mounting, the number of green fluorescent cells was counted under a fluorescence microscope (green fluorescent cells represent beta-like cells that transdifferentiate from alpha cells).

[0055] Experimental results are as follows Figure 2-3 As shown. Among them, Figure 3 This is a cell fluorescence imaging diagram showing how flavonoids promote the transdifferentiation of pancreatic alpha cells into beta cells in this embodiment. Figure 3 This is a bar chart illustrating the effect of limonene flavonoids on the transdifferentiation of pancreatic alpha cells into beta cells in this embodiment; from Figure 2-3 It can be seen that 5-Hydroxy-6,7-dimethoxylflavone has the ability to promote the transdifferentiation of pancreatic alpha cells into beta cells.

[0056] Example 3: 5-Hydroxy-6,7-dimethoxylflavone exhibits hypoglycemic effect in a diabetic zebrafish model. (I) Construction of a diabetic zebrafish model and detection of free glucose: Transgenic zebrafish Tg (Ins:htBidTE-ON;LR) were divided into three groups: Control group, DMSO group, and purslane brass group. The pancreatic beta cells of transgenic zebrafish Tg(Ins:htBidTE-ON;LR) in the Control group were not induced to ablate, and their blood glucose levels were normal. Transgenic zebrafish Tg (Ins:htBidTE-ON;LR) from the tadalafil brass group were induced with doxycycline and tebufenozide in zebrafish embryo culture medium, and the pancreatic beta cells were ablated. The beta cells were destroyed by induction, and then treated with 2.5 μM (final concentration) tadalafil flavonoid solution (dissolved in DMSO).

[0057] In zebrafish Tg (Ins:htBidTE-ON;LR) transgenic zebrafish in the DMSO group, pancreatic beta cells were ablated after induction with the compounds doxycycline and tebufenozide in zebrafish embryo culture medium. Then, the same volume of DMSO as the flavonoid group was added for treatment to construct a diabetic zebrafish model. The beta cells of the transgenic zebrafish Tg (Ins:htBidTE-ON;LR) in the DMSO group were destroyed after induction, and blood glucose rose sharply. It was regarded as a diabetic zebrafish model. The transgenic zebrafish from the above groups were cultured for 24 h, and then total glucose was determined. Total glucose was determined using the Amplex glucose / glucose oxidase assay kit. Ten zebrafish larvae from each group were homogenized in 100 μl of sample buffer. After homogenization in 1.5 ml centrifuge, the mixture was centrifuged at 12000 rpm for 10 minutes at 4°C. Free glucose in 10 μl of the supernatant (equivalent to the amount of one larva) was measured according to the kit instructions. Each sample was subjected to at least three biological replicates. The experimental results are as follows: Figure 4 As shown. Figure 4 This is a bar chart showing the hypoglycemic effect of purslane flavonoids in a diabetic zebrafish model in this embodiment. This experiment demonstrates that the alpha cell transdifferentiation and beta cell regeneration promoted by purslane flavonoids produce functional new beta cells that can lower blood sugar.

[0058] Example 4: 5-Hydroxy-6,7-dimethoxylflavone promotes the transdifferentiation of alpha cells into beta cells by enhancing pdx1 expression. (1) Cell culture: αTC1-6 cells (mouse insulinoma pancreatic islet α cell line) were cultured in Dulbecco's Modified Eagle Medium (DMEM) low-glucose medium (PM150220, Pricella) supplemented with 10 mM HEPES (15630080, Gibco), 100 U / mL penicillin, 0.1 mg / mL streptomycin (E607011-0100, BBI), and 10% fetal bovine serum (FBS, 164210-50, Pricella) at 37°C in a 5% CO2 humidified incubator.

[0059] (2) Dual-luciferase reporter gene detection: αTC1-6 cells were seeded in 96-well plates and cultured overnight. The cells were then divided into three groups: a control group transfected with the empty reporter plasmid pGL6, a DMSO group transfected with the reporter plasmid pGL6-Pdx1 and treated with DMSO, and a meropenem group transfected with the reporter plasmid pGL6-Pdx1 and treated with meropenem. In the control group, the reporter plasmid (pGL6) and the internal control plasmid vector (pRL-SV40-C) were transfected into αTC1-6 cells using PEI transfection reagent (24765, Polysciences). Transfecting reporter plasmid pGL6-Pdx1 and treating with DMSO (DMSO group): αTC1-6 cells were transfected with pGL6-Pdx1 reporter plasmid and internal control plasmid vector (pRL-SV40-C) using PEI transfection reagent (24765, Polysciences). 24 hours after transfection, the cells were treated with the same volume of DMSO as the flavonoid group. The reporter plasmid pGL6-Pdx1 and the treatment group with citrus flavonoids (citrus flavonoid group) were transfected into αTC1-6 cells using PEI transfection reagent (24765, Polysciences) to include the pGL6-Pdx1 reporter plasmid and the internal control plasmid vector (pRL-SV40-C). Twenty-four hours after transfection, cells were treated with 2.5 μM (final concentration) citrus flavonoid solution.

[0060] After 24 hours of treatment, luciferase activity was measured using a dual-luciferase reporter gene assay kit (RG088S, Beyotime). Each experiment was performed in triplicate, with at least three replicates per group.

[0061] Experimental results are as follows Figure 5 As shown. Figure 5 This is a bar chart showing the effect of flavonoids from *Cephalotaxus fortunei* on the Pdx1 gene in the alpha cell line in this embodiment.

[0062] Conclusion: This invention uses zebrafish as a model to determine the transdifferentiation number of pancreatic alpha cells. Furthermore, a free glucose assay kit was used to detect the hypoglycemic effect of the drug in diabetic zebrafish, and the potential target of the drug in promoting the transdifferentiation of pancreatic alpha cells into beta cells was explored. Experimental results demonstrate that 5-Hydroxy-6,7-dimethoxylflavone can promote the transdifferentiation of pancreatic alpha cells into beta cells. The drug, when present in the pancreatic alpha cell line, can promote the expression of Pdx1 in alpha cells, which is a potential mechanism for transdifferentiation into beta cells.

[0063] The foregoing has described and evaluated some embodiments of the present invention. It should be understood that the present invention is not limited to the specific embodiments described above. Any person skilled in the art can make many possible variations and modifications to the technical solutions of the present invention, or modify them into equivalent embodiments, without departing from the scope of the present invention. This does not affect the essential content of the present invention. Therefore, any simple modifications, equivalent changes, and modifications made to the above embodiments based on the technical essence of the present invention, without departing from the content of the present invention, still fall within the protection scope of the present invention.

Claims

1. Application of flavonoids in the preparation of hypoglycemic drugs, drugs for the prevention or treatment of diabetes, or functional foods that assist in lowering blood sugar in patients with hyperglycemia or diabetes.

2. The application according to claim 1, characterized in that, The flavonoids from the purslane promote the regeneration of pancreatic beta cells.

3. The application according to claim 2, characterized in that, The flavonoids from the flavonoids promote the transdifferentiation of pancreatic alpha cells into beta cells.

4. The application according to any one of claims 1-3, characterized in that, The diabetes includes type 1 diabetes, type 2 diabetes, gestational diabetes, or special types of diabetes.

5. The application according to claim 4, characterized in that, The flavonoids from the purslane act on the Pdx1 gene, enhancing the function of pancreatic beta cells.

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