Medical repair hydrogel and preparation method thereof

Abstract

This invention discloses a medical repair hydrogel and its preparation method, specifically relating to the field of biomedical engineering technology. The hydrogel is a three-dimensional network structure formed by the synergistic self-assembly of glycyrrhizic acid and polydipsia glycoside through non-covalent bonds such as hydrogen bonding, hydrophobic interactions, and π-π stacking. No chemical cross-linking agent is required. It spontaneously forms a hydrogel upon heating to 70°C until completely dissolved and then cooling. It possesses reactive oxygen species-responsive structural dissociation characteristics, mechanical properties adapted to myocardial tissue, and a controllable degradation rate. This invention is suitable for intramyocardial drug administration after PCI, avoiding the shortcomings of traditional synthetic hydrogels that require external triggering and have unsuitable gelation conditions. Simultaneously, its three-dimensional network structure enables simultaneous long-term sustained release of the two active ingredients, with a 24-hour burst release rate of less than 25% and a cumulative release rate exceeding 70% within 7 days. This solves the problem of short half-lives and rapid clearance by body fluids of small molecule drugs, achieving continuous drug delivery to the lesion site.

Description

Technical Field

[0001] This invention relates to the field of biomedical engineering, and in particular to a medical repair hydrogel and its preparation method. Background Technology

[0002] Myocardial infarction is a serious cardiovascular emergency that threatens human life and health. Its pathological process involves multiple complex intertwined processes, including oxidative stress, inflammatory response, apoptosis, and fibrotic remodeling. Percutaneous coronary intervention (PCI) is the core clinical treatment for acute myocardial infarction, rapidly opening occluded vessels and restoring myocardial blood flow. However, this therapy cannot reverse existing myocardial cell necrosis, nor can it effectively block subsequent ventricular remodeling. Postoperative structural repair and functional recovery of myocardial tissue remain critical clinical challenges. Against this backdrop, hydrogel materials, possessing a three-dimensional porous structure, good biocompatibility, and injectability, have become a research hotspot in the field of myocardial repair, considered ideal tissue-engineered scaffolds capable of filling infarct defects and regulating the local pathological microenvironment.

[0003] Current hydrogel technologies for myocardial repair generally have significant shortcomings, making it difficult to meet the actual needs of clinical treatment. One type is drug-loaded hydrogels, which use carboxymethyl chitosan, synthetic peptides, etc., as inert carriers to load single-function drugs or biological factors through physical embedding or chemical grafting. This is a simple "carrier + drug" combination, which suffers from a disconnect between structure and therapeutic function. Not only is drug release poorly controllable, but it also cannot simultaneously intervene in the complex pathological network of multiple stages after myocardial infarction. Another type is synthetic polymer hydrogels, which rely on chemical cross-linking agents to achieve gelation, posing a biocompatibility risk due to residual cross-linking agents. Furthermore, their mechanical properties are not well-suited to myocardial tissue, easily causing secondary damage to damaged myocardium. In addition, while stem cell / exosome combined hydrogel treatment strategies theoretically possess multi-effect repair potential, they face challenges such as low cell survival rates, unclear mechanisms of action, difficulties in production standardization, and potential immune rejection and tumorigenesis risks, resulting in extremely high barriers to clinical translation.

[0004] The core challenge of current technology lies in the lack of an integrated myocardial repair material that organically combines material structure with therapeutic function, while also possessing multi-target synergistic effects, excellent biocompatibility, and clinical translational feasibility. Existing technologies are either single-function, targeting only one link in the pathological chain of myocardial infarction, or have complex systems with high safety risks or production and application costs, failing to achieve systematic and efficient repair of myocardial infarction. Therefore, developing a novel intelligent hydrogel with "structure as function," overcoming the limitations of traditional "drug delivery separation" technology, has become a key direction for solving the myocardial repair problem after myocardial infarction. Summary of the Invention

[0005] The main objective of this invention is to provide a medical repair hydrogel and its preparation method, which can effectively solve the problems involved in the above-mentioned background art.

[0006] To achieve the above objectives, the technical solution adopted by the present invention is as follows: A medical repair hydrogel, wherein the repair hydrogel is formed by the non-covalent self-assembly of glycyrrhizic acid and polydipsia glycoside to form a three-dimensional network structure; The mass ratio of glycyrrhizic acid to polygalactoside is from 15 mg:0.5 mg to 60 mg:2 mg, and the total concentration is from 1.55% to 6.2% (w / v). The non-covalent interactions include hydrogen bonding, hydrophobic interactions, and π-π stacking. After being heated to 70°C until completely dissolved and then cooled, the glycyrrhizic acid and polygalactosin can spontaneously assemble into nanofibers or nanoribbons that entangle and crosslink to form a hydrogel. The hydrogel is responsive to the highly reactive oxygen species (ROS) microenvironment in the myocardial infarction area and undergoes structural dissociation in an environment with an ROS concentration ≥100 μM.

[0007] Preferably, the mass ratio of glycyrrhizic acid to polygalactoside is 30 mg: 1 mg; the total concentration of the hydrogel is preferably 3.1% (w / v), it dissolves at 70°C and rapidly gels upon cooling, and its storage modulus is 500-1000 Pa. The storage modulus of the hydrogel matches that of myocardial tissue. The degradation time of the hydrogel is 7-28 days; Once the hydrogel is pre-prepared, it can be injected into the body using a 27G-30G minimally invasive injection needle.

[0008] Preferably, the hydrogel is administered via the following steps: the prepared hydrogel is injected at three points in the myocardial infarction area and the junction after percutaneous coronary intervention (PCI) using a cardiac catheter, with each injection volume being 5-10 μL. An antiplatelet drug is used in combination with the medication, which is administered 1-2 hours before the hydrogel injection.

[0009] A method for preparing a medical repair hydrogel, comprising the following steps: S1. Glycyrrhizic acid was dissolved in phosphate-buffered saline (PBS) at pH 7.4 and sonicated to aid dissolution, thus obtaining a glycyrrhizic acid stock solution; Polygonum cuspidatum glycoside was dissolved in PBS at pH 7.4 and sonicated to aid dissolution, thus obtaining a polygonum cuspidatum glycoside stock solution. S2. At room temperature, mix glycyrrhizic acid stock solution and polygala glycoside stock solution at a mass ratio of 15 mg: 0.5 mg to 60 mg: 2 mg, add PBS to the preset total concentration, and gently vortex to mix. S3. Heat the mixed solution to 70°C until completely dissolved, and after cooling, form a self-assembled hydrogel; no chemical cross-linking agent or initiator is added during the entire preparation process.

[0010] Preferably, the mass ratio of glycyrrhizic acid to polygalactoside in S2 is 30 mg: 1 mg.

[0011] Preferably, the concentration of the glycyrrhizic acid stock solution in S1 is 30 mg / mL.

[0012] Preferably, the total concentration of the mixed solution in S2 is 3.1% (w / v).

[0013] Compared with the prior art, the present invention has the following beneficial effects: 1. This invention requires no chemical cross-linking agent. Relying on the non-covalent self-assembly of glycyrrhizic acid and polygalactosyl glycoside, it dissolves at 70°C and gels upon cooling, forming a stable three-dimensional network structure with a storage modulus of 500-1000 Pa. The pre-prepared hydrogel has a suitable viscosity, allowing for minimally invasive catheter injection via 27G-30G needles, perfectly suited for intramyocardial drug administration after PCI, avoiding the shortcomings of traditional synthetic hydrogels that require external triggering and have unsuitable gelation conditions. Simultaneously, its three-dimensional network structure enables simultaneous long-term sustained release of the two active ingredients, with a 24-hour burst release rate of less than 25% and a cumulative release rate exceeding 70% within 7 days. This solves the problem of short half-lives and rapid clearance by body fluids of small molecule drugs, achieving continuous drug delivery to the lesion site.

[0014] 2. This invention overcomes the limitations of single-component, single-target treatment. Through the synergistic combination of glycyrrhizic acid and polygala glycoside, it simultaneously exerts antioxidant, anti-apoptotic, and anti-fibrotic effects at the cellular level. In an H2O2-induced cardiomyocyte oxidative stress model, the glycyrrhizic acid-polygala glycoside self-assembled hydrogel extract increased cell activity to 88.5%, significantly better than the glycyrrhizic acid monotherapy group, while reducing the late-stage apoptosis rate to 12.3%, a significantly greater reduction than the single-component treatment group. In a cardiac fibroblast activation model, this glycyrrhizic acid-polygala glycoside self-assembled hydrogel inhibited approximately 70% of α-SMA expression upregulation, significantly reduced collagen secretion, and blocked the fibrosis process at its source, forming a networked intervention against the pathological aspects of myocardial infarction.

[0015] 3. After minimally invasive injection, this invention can increase left ventricular ejection fraction by 15-20% and reduce the area of ​​fibrotic scarring in the infarct zone by 30-40% 7 days post-surgery. It also promotes angiogenesis in the infarct border area, demonstrating a comprehensive improvement effect superior to the saline group and the glycyrrhizic acid monotherapy group. Compared to traditional monotherapy-loaded hydrogels and stem cell therapies, this invention's glycyrrhizic acid-polygonum cuspidatum self-assembled hydrogel achieves systematic regulation of the "oxidative stress-cell death-fibrosis" pathological chain. Furthermore, its core components are derived from natural Chinese medicine, exhibiting excellent biocompatibility. No abnormal inflammatory infiltration, granulomas, or calcification were observed at the injection site, and no toxic damage was observed to major organs. This avoids the safety concerns of synthetic materials and the potential risks of cell therapy, possessing extremely high clinical translational value. Attached Figure Description

[0016] Figure 1 This is a flowchart of the preparation method of the present invention. Detailed Implementation

[0017] To make the technical means, creative features, objectives and effects of this invention easier to understand, the invention will be further described below in conjunction with specific embodiments.

[0018] This invention discloses a medical repair hydrogel for minimally invasive interventional treatment of myocardial infarction and its preparation method. The core of this invention is the non-covalent self-assembly of glycyrrhizic acid and polydipsia glycoside, two natural active small molecules, to construct an intelligent hydrogel system that combines structural support and synergistic therapeutic functions. The invention is described in detail below with specific embodiments. The materials used include glycyrrhizic acid with a purity ≥98%, polydipsia glycoside with a purity ≥98%, and phosphate-buffered saline (PBS). Characterization methods include testing the storage modulus and loss modulus of the gel using a rheometer, observing the microstructure of the gel using scanning electron microscopy, determining the drug release pattern using high-performance liquid chromatography, using the H9C2 cardiomyocyte cell line and primary cardiac fibroblasts for cell experiments, and using a C57BL / 6 mouse myocardial infarction model for animal experiments. All animal procedures followed relevant guidelines from the Animal Ethics Committee.

[0019] Example 1: This example aims to verify the necessity of glycyrrhizic acid and polygalactosidase synergistic self-assembly into a gel, and to clarify the physicochemical properties, mechanical compatibility, degradation rate regulation characteristics, and reactive oxygen species (ROS) responsiveness of the hydrogel.

[0020] The hydrogel is a three-dimensional network structure formed by the self-assembly of glycyrrhizic acid and polygalactoside through non-covalent bonds such as hydrogen bonding, hydrophobic interaction and π-π stacking. The mass ratio of glycyrrhizic acid to polygalactoside is from 15mg:0.5mg to 60mg:2mg, preferably 30mg:1mg. The total concentration of the two components is from 1.55% to 6.2% (w / v). It can spontaneously gel after being heated to 70°C until completely dissolved and cooled.

[0021] In the specific preparation example 1: Weigh 30.0 mg of glycyrrhizic acid and 1.0 mg of polygalactoside, with a mass ratio of 30 mg: 1 mg, add 1.0 mL of pH 7.4 phosphate buffer, vortex to fully premix, heat the mixed solution at 70 °C until completely dissolved, and after cooling, form a self-assembled hydrogel. The total concentration of this sample is 3.1% (w / v). Preparation Example 2: Weigh 15.0 mg of glycyrrhizic acid and 0.5 mg of polygalactoside, with a mass ratio of 30 mg: 1 mg. Proceed as described above. The total concentration is 1.55% (w / v). Preparation Example 3: Weigh 60.0 mg of glycyrrhizic acid and 2.0 mg of polygalactoside, with a mass ratio of 30 mg: 1 mg. Proceed as described above. The total concentration is 6.2% (w / v).

[0022] For comparison, Comparative Example 1 and Comparative Example 2 were set up. In Comparative Example 1, only 31.0 mg of glycyrrhizic acid was dissolved in 1.0 mL of PBS, and after being treated in the same way, an injectable self-assembled hydrogel was formed after standing. In Comparative Example 2, only 1.0 mg of Polygonum cuspidatum glycoside was dissolved in 1.0 mL of PBS, and after being treated in the same way, the solution remained clear and no gelation occurred.

[0023] Experimental results show that glycyrrhizic acid, as an amphiphilic molecule, is the driving force for the formation of nanostructures. The aromatic ring structure of Polygonum cuspidatum and the hydrophobic core of glycyrrhizic acid combine through hydrophobic interactions and π-π stacking to jointly drive and stabilize the formation of the three-dimensional network structure; a single component cannot form a gel. Gelation tests show that all prepared samples with different ratios completed gelation after being heated to 70℃ and cooled. Among them, the prepared sample with a mass ratio of 30mg:1mg showed stable gelation and was fully suitable for clinical injection procedures.

[0024] Rheological property testing was conducted at a frequency of 1 Hz and a strain of 1%. Results showed that the storage modulus of the samples prepared with different ratios ranged from 500 to 1000 Pa. Sample prepared as Example 1 had a storage modulus of approximately 850 Pa and a loss modulus of approximately 120 Pa, exhibiting typical elasticity. This storage modulus range matches the modulus of myocardial tissue, indicating that injection will not interfere with myocardial contractile function. Furthermore, the mechanical strength of the gel can be precisely controlled within a certain range by adjusting the mass ratio of the two components. Scanning electron microscopy revealed that the lyophilized sample prepared as Example 1 exhibited an interconnected porous three-dimensional network structure with pore sizes of approximately 50-200 μm, which is beneficial for nutrient exchange and cell migration.

[0025] Further degradation experiments showed that the degradation time of the glycyrrhizic acid polygalactosidase self-assembled hydrogel could be controlled by the total concentration. The degradation time was 7 days when the total concentration was 1.55% (w / v), 14 days when the total concentration was 3.1% (w / v), and 28 days when the total concentration was 6.2% (w / v), which can match the different treatment needs of the acute and repair phases of myocardial infarction.

[0026] ROS responsiveness testing showed that the hydrogel underwent structural dissociation in an environment with a reactive oxygen species concentration ≥100 μM, providing a structural basis for targeted drug release.

[0027] Example 2 aims to verify the sustained-release performance, ROS-responsive drug release characteristics, and synergistic therapeutic effect of the hydrogel at the cellular level. The drug release experiment used the sample from Preparation Example 1, placed it in a dialysis bag, and immersed it in PBS release medium (pH 7.4) containing 0.5% Tween 80 to maintain the leak conditions. The mixture was kept at a constant temperature of 37°C with shaking. Samples were taken at preset time points, and the concentrations of glycyrrhizic acid and polygalactosyl glycoside in the medium were determined by high-performance liquid chromatography (HPLC). The cumulative release rate was calculated.

[0028] Experimental results showed that glycyrrhizic acid and polygalactosin exhibited highly synchronized sustained-release behavior, with burst release rates of 22.1%±3.5% and 20.8%±2.9% at 24 h, respectively. Subsequently, they were released slowly and continuously over a period of up to 7 days, with final cumulative release rates of 73.2%±6.5% and 70.1%±5.1%, respectively, demonstrating the excellent encapsulation and controlled release capability of the gel network for both molecules. In a simulated myocardial infarction microenvironment with reactive oxygen species concentrations ≥100 μM, the hydrogel structure dissociated more rapidly, increasing the drug release rate and further validating its targeted drug release characteristics.

[0029] In vitro cell experiments were conducted using experimental group 1, experimental group 2, a positive control group, and a normal control group. Experimental group 1 consisted of H9C2 cardiomyocytes treated with 200 μM H2O2 to induce oxidative stress damage, and the extract of sample preparation example 1 was added. This extract was obtained by soaking glycyrrhizic acid-polysaccharide self-assembled hydrogel in culture medium for 24 h. Experimental group 2 consisted of H9C2 cardiomyocytes treated with 200 μM H2O2 to induce oxidative stress damage, and the extract containing glycyrrhizic acid monomer hydrogel was added. This extract was obtained by soaking glycyrrhizic acid monomer hydrogel in culture medium for 24 h. The positive control group consisted of H9C2 cardiomyocytes treated with only 200 μM H2O2. The normal control group consisted of normal H9C2 cardiomyocytes that were not treated with H2O2.

[0030] After 24 hours of treatment, cell viability was assessed using the CCK-8 assay, and apoptosis rate was detected by flow cytometry. The results showed that cell viability in the positive control group decreased to 52.3% ± 5.1% of the normal control group. The glycyrrhizic acid monotherapy group increased cell viability to 78.6% ± 6.2%, while the glycyrrhizic acid-polygonum cuspidatum self-assembled hydrogel extract group exhibited a stronger protective effect, significantly increasing cell viability to 88.5% ± 4.7%, and this group showed a statistically significant difference compared to the glycyrrhizic acid monotherapy group. Apoptosis rate detection showed that H2O2 induced a late-stage apoptosis rate of 35.4% ± 3.8%, which was reduced by glycyrrhizic acid monotherapy to 19.1% ± 2.5%, while the glycyrrhizic acid-polygonum cuspidatum self-assembled hydrogel extract further reduced it to 12.3% ± 1.9%, showing a statistically significant difference compared to the glycyrrhizic acid monotherapy group. Meanwhile, in the TGF-β1-induced cardiac fibroblast activation model, treatment with glycyrrhizic acid polygalactosidase self-assembled hydrogel extract can inhibit the upregulation of α-SMA expression by about 70%, and significantly reduce the secretion of collagen I and III. This effect is also better than that of the single-component treatment group, which confirms that the hydrogel has excellent synergistic effects of anti-oxidation, anti-apoptosis and anti-fibrosis.

[0031] Example 3: This example aims to verify the in vivo therapeutic effect, biocompatibility, and feasibility of the clinical dosing regimen of the hydrogel of the present invention using animal models. During the experiment, C57BL / 6 mice were randomly divided into 4 groups of 8 mice each: sham operation group, myocardial infarction model + saline group, myocardial infarction model + glycyrrhizic acid monotherapy group, and myocardial infarction model + hydrogel of the present invention group. The myocardial infarction model was established by permanently ligating the left anterior descending artery.

[0032] The preparation process of this hydrogel does not require the addition of any chemical cross-linking agent or initiator. The specific steps are as follows: First, prepare the stock solution by dissolving glycyrrhizic acid in phosphate buffered saline (PBS) at pH 7.4 and sonicating it to obtain a glycyrrhizic acid stock solution with a concentration of 30 mg / mL. Then, dissolve polydipsia glycoside in PBS at pH 7.4 and sonicate it to obtain a polydipsia glycoside stock solution. Subsequently, at room temperature, mix the glycyrrhizic acid stock solution and the polydipsia glycoside stock solution according to the ratio of Preparation Example 1, add PBS to the preset total concentration, and gently vortex to mix. Finally, heat the mixed solution to 70°C until completely dissolved, and after cooling, a self-assembled hydrogel is formed.

[0033] During treatment, medication was administered three days post-ligation. Under direct vision, a 30G insulin needle was used to inject the prepared hydrogel at three points along the infarct edge, with each point receiving 5-10 μL. The hydrogel group received 20 μL of the hydrogel prepared in Example 1; the free drug group received a solution containing equal volumes of glycyrrhizic acid and polygalactoside; and the saline group received an equal volume of saline. In the hydrogel group, antiplatelet drugs were administered to mice 1-2 hours prior to injection to jointly reduce the risk of restenosis post-surgery.

[0034] Seven days after administration, mice in each group were comprehensively evaluated. Echocardiography showed that the left ventricular ejection fraction decreased to 38.5%±3.2% in the myocardial infarction model + saline group, partially recovered to 45.2%±4.1% in the glycyrrhizic acid monotherapy group, and significantly increased to 53.8%±3.6% in the hydrogel group of this invention. This data showed a highly statistically significant difference compared with the saline group and a statistically significant difference compared with the glycyrrhizic acid monotherapy group. At the same time, the expansion of left ventricular end-diastolic volume was significantly inhibited.

[0035] Histological analysis using Masson's trichrome staining showed that the fibrotic scar area in the infarct region was 42.7% ± 4.5% in the saline group, 35.1% ± 3.8% in the glycyrrhizic acid monotherapy group, and significantly reduced to 28.3% ± 3.1% in the hydrogel group. TUNEL staining showed that the number of apoptotic cardiomyocytes in the infarct margin region of the glycyrrhizic acid-polygonum cuspidatum self-assembled hydrogel group was significantly lower than that in the saline group and the glycyrrhizic acid monotherapy group. CD31 immunofluorescence staining showed that the microvessel density in the infarct margin region of the glycyrrhizic acid-polygonum cuspidatum self-assembled hydrogel group was significantly higher than that in the other two model groups.

[0036] Molecular biological analysis showed that the level of MDA, a marker of oxidative stress, was significantly reduced in the infarcted myocardial tissue of the glycyrrhizic acid-polysaccharide self-assembled hydrogel group, the activity of endogenous antioxidant enzyme SOD was enhanced, and the mRNA expression of profibrotic factors TGF-β1 and CollagenI was significantly downregulated, confirming that the hydrogel achieved synchronous and synergistic intervention on the pathological chain of "oxidative stress-cell death-fibrosis".

[0037] Biocompatibility testing showed that there was no obvious abnormal inflammatory cell infiltration, foreign body granuloma formation, or tissue calcification at the hydrogel injection site. H&E staining of major organs such as the heart, liver, spleen, lungs, and kidneys of mice showed no obvious pathological changes, and blood biochemical indicators were all within the normal range, proving that the hydrogel has excellent in vivo biocompatibility.

[0038] In summary, the glycyrrhizic acid / polygonum cuspidatum self-assembled smart hydrogel of the present invention achieves the integration of structure and function through the synergistic self-assembly of natural active ingredients. It has the characteristics of ROS-responsive targeted drug release, controllable degradation rate, and mechanical properties adapted to myocardial tissue. At the same time, combined with the post-PCI injection site-specific administration regimen and the combined administration of antiplatelet drugs, it shows significant myocardial repair effects and clinical translation potential.

[0039] The foregoing has shown and described the basic principles, main features, and advantages of the present invention. Those skilled in the art should understand that the present invention is not limited to the above embodiments. The embodiments and descriptions in the specification are merely illustrative of the principles of the invention. Various changes and modifications can be made to the invention without departing from its spirit and scope, and all such changes and modifications fall within the scope of the present invention as claimed. The scope of protection of this invention is defined by the appended claims and their equivalents.

[0040] The foregoing has shown and described the basic principles, main features, and advantages of the present invention. Those skilled in the art should understand that the present invention is not limited to the above embodiments. The embodiments and descriptions in the specification are merely illustrative of the principles of the invention. Various changes and modifications can be made to the invention without departing from its spirit and scope, and all such changes and modifications fall within the scope of the present invention as claimed. The scope of protection of this invention is defined by the appended claims and their equivalents.

Claims

1. A medical repair hydrogel, characterized in that: The repair hydrogel is formed by the non-covalent self-assembly of glycyrrhizic acid and Polygonum cuspidatum glycosides to form a three-dimensional network structure; The mass ratio of glycyrrhizic acid to polygalactoside is from 15 mg:0.5 mg to 60 mg:2 mg, and the total concentration is from 1.55% to 6.2% (w / v). The non-covalent interactions include hydrogen bonding, hydrophobic interactions, and π-π stacking. After being heated to 70°C until completely dissolved and then cooled, the glycyrrhizic acid and polygalactosidase can spontaneously assemble into nanofibers or nanoribbons and entangle and crosslink to form a hydrogel. The hydrogel is responsive to the highly reactive oxygen species (ROS) microenvironment in the myocardial infarction area and undergoes structural dissociation in an environment with an ROS concentration ≥100 μM.

2. The medical repair hydrogel according to claim 1, characterized in that: The preferred mass ratio of glycyrrhizic acid to polygalactoside is 30 mg: 1 mg; The total concentration of the hydrogel is preferably 3.1% (w / v), which dissolves upon heating at 70°C and rapidly gels upon cooling, with a storage modulus of 500-1000 Pa. The storage modulus of the hydrogel matches that of myocardial tissue. The degradation time of the hydrogel is 7-28 days; The hydrogel precursor solution can be injected with a 27G-30G minimally invasive injection needle to form a gel in situ in vivo.

3. The medical repair hydrogel according to claim 1, characterized in that: The specific steps for administering the hydrogel are as follows: After percutaneous coronary intervention (PCI), the prepared hydrogel is injected at three points in the myocardial infarction area and junction through a cardiac catheter, with an injection volume of 5-10 μL at each point; antiplatelet drugs are used in conjunction with the hydrogel, and the antiplatelet drugs are administered 1-2 hours before the hydrogel injection.

4. A method for preparing a medical repair hydrogel, used to prepare the medical repair hydrogel according to any one of claims 1-3, characterized in that: Includes the following steps: S1. Glycyrrhizic acid was dissolved in phosphate-buffered saline (PBS) at pH 7.4 and sonicated to aid dissolution, thus obtaining a glycyrrhizic acid stock solution; Polygonum cuspidatum glycoside was dissolved in PBS at pH 7.4 and sonicated to aid dissolution, thus obtaining a polygonum cuspidatum glycoside stock solution. S2. At room temperature, mix glycyrrhizic acid stock solution and polygala glycoside stock solution at a mass ratio of 15 mg: 0.5 mg to 60 mg: 2 mg, add PBS to the preset total concentration, and gently vortex to mix. S3. Heat the mixed solution to 70°C until completely dissolved, and after cooling, form a self-assembled hydrogel.

5. The method for preparing medical repair hydrogel according to claim 4, characterized in that: The preferred mass ratio of glycyrrhizic acid to polygalactoside in S2 is 30 mg: 1 mg.

6. The method for preparing medical repair hydrogel according to claim 4, characterized in that: The concentration of the glycyrrhizic acid stock solution described in S1 is 30 mg / mL.

7. The method for preparing medical repair hydrogel according to claim 4, characterized in that: The total concentration of the mixed solution described in S2 is 1.55% to 6.2% (w / v).

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