Method and device for determining influence of targeted acyltransferase P300 on myocardial internal hemorrhage injury

Abstract

The invention provides a method and device for determining the influence of targeted acyltransferase P300 on myocardial internal hemorrhage injury, electronic equipment and a storage medium, and relates to the technical field of biomedicine. The method comprises the following steps: if specific protein acted by P300 exists in myocardial tissue, determining whether the specific protein has the influence of the P300 on the lactoacylation level or not; if it is determined that the influence of the milk acylation level exists, the information of the influence of the milk acylation level on the myocardial internal hemorrhage injury is determined through an experimental subject added with an expression quantity regulator. According to the invention, the influence on myocardial internal hemorrhage injury can be determined by determining whether the P300 has the influence on the milk acylation level of the myocardial tissue or not.

Description

Technical Field

[0001] The present disclosure relates to the field of biomedical technology, and in particular to a method and device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury. Background Art

[0002] Myocardium is the main muscle tissue that makes up the heart wall. It has the functions of contraction and relaxation and transports blood to various organs throughout the body. Myocardial injury refers to the invasion of myocardial cells by various harmful factors, which leads to structural and functional disorders, and even necrosis and apoptosis.

[0003] If myocardial injury is to be treated, the influencing factors of myocardial injury must be found first. Therefore, how to determine the influencing factors of myocardial injury is a technical problem that needs to be solved urgently in this field. Summary of the invention

[0004] In view of this, the purpose of the present disclosure is to propose a method and device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury. The present disclosure can solve the existing problems in a targeted manner.

[0005] Based on the above-mentioned purpose, in a first aspect, the present disclosure proposes a method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury, comprising: if there is a specific protein that P300 acts on in myocardial tissue, determining whether P300 has an effect on the lactylation level of the specific protein; if it is determined that there is an effect on the lactylation level, determining the effect information of the lactylation level on intramyocardial hemorrhage injury by adding an experimental subject to an expression regulator.

[0006] In the second aspect, a device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage damage is also provided, comprising: a first determination unit, configured to determine whether P300 has an effect on the lactylation level of a specific protein if the specific protein it acts on exists in myocardial tissue; a second determination unit, configured to determine the effect information of the lactylation level on intramyocardial hemorrhage damage by adding an expression regulator to an experimental subject if it is determined that there is an effect on the lactylation level.

[0007] According to a third aspect, an electronic device is provided, comprising a memory, a processor, and a computer program stored in the memory and executable on the processor, wherein the processor executes the computer program to implement the method described in the first aspect.

[0008] According to a fourth aspect, a computer-readable storage medium is provided, on which a computer program is stored, and the program is executed by a processor to implement any method described in the first aspect.

[0009] In general, the present disclosure has at least the following beneficial effects: it can provide a method for determining whether P300 has an effect on intramyocardial hemorrhage injury. By determining whether P300 has an effect on the lactylation level of myocardial tissue, the effect on intramyocardial hemorrhage injury is determined. BRIEF DESCRIPTION OF THE DRAWINGS

[0010] In the accompanying drawings, unless otherwise specified, the same reference numerals throughout the multiple drawings represent the same or similar parts or elements. These drawings are not necessarily drawn to scale. It should be understood that these drawings only depict some embodiments disclosed in accordance with the present disclosure and should not be regarded as limiting the scope of the present disclosure.

[0011] Figure 1 A flow chart of a method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury according to an embodiment of the present disclosure is shown;

[0012] Figure 2 A flow chart for determining the lactylation modification sites regulated by the P300 is shown;

[0013] Figure 3a The molecular mechanism of p300 lactylation modification of key proteins in the border zone of STEMI reperfusion intramyocardial hemorrhage according to the embodiments of the present disclosure is shown;

[0014] Figure 3b A flow chart is shown for determining the role of p300-regulated key protein lactylation modification in STEMI reperfusion intramyocardial hemorrhage injury according to an embodiment of the present disclosure;

[0015] Figure 3c A flowchart showing the role of key protein lactylation modifications in STEMI reperfusion intramyocardial hemorrhage injury;

[0016] Figure 4 A schematic diagram of a device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury according to an embodiment of the present disclosure is shown;

[0017] Figure 5 A schematic diagram of the structure of an electronic device provided by an embodiment of the present disclosure is shown;

[0018] Figure 6 A schematic diagram of a storage medium provided by an embodiment of the present disclosure is shown. DETAILED DESCRIPTION

[0019] The present disclosure is further described in detail below in conjunction with the accompanying drawings and embodiments. It is understood that the specific embodiments described herein are only used to explain the relevant invention, rather than to limit the invention. It is also necessary to explain that, for ease of description, only the parts related to the relevant invention are shown in the accompanying drawings.

[0020] It should be noted that, in the absence of conflict, the embodiments and features in the embodiments of the present disclosure may be combined with each other. The present disclosure will be described in detail below with reference to the accompanying drawings and in combination with the embodiments.

[0021] Figure 1 The method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury disclosed in the present invention is shown. In an embodiment of the present invention, the method comprises:

[0022] Step S101, if the specific protein acted by P300 exists in the myocardial tissue, it is determined whether the P300 has an effect on the lactylation level of the specific protein.

[0023] In this embodiment, the subject of the method for determining the effect of lactacyl transferase targeting acyl transferase P300 on intramyocardial hemorrhage injury can determine whether there is a specific protein in myocardial tissue that P300 acts on. The subject can be any electronic device such as a terminal device.

[0024] For example, the above-mentioned execution entity can first perform spatial lactylation modification omics to screen for differential protein lactylation sites in the peri-infarct boundary zone: protein samples from the beagle dog reperfusion infarction zone (hemorrhagic zone), peri-infarct zone, and normal left ventricular myocardial tissue are respectively hydrolyzed into a peptide mixture, and then the hydrolyzed peptide mixture is separated by liquid chromatography, and then the modified peptides are enriched by high-quality lactylation modification antibodies and biological materials, and finally liquid chromatography-tandem mass spectrometry is used for quantitative analysis to screen for specific protein lactylation modification sites in the peri-infarct boundary zone.

[0025] The execution subject can determine whether P300 has an effect on the lactylation level of the specific protein in various ways. For example, the expression level of P300 in the experimental subject is adjusted, and the lactylation level of the specific protein is detected. If the lactylation level is different from the conventional lactylation level of the specific protein, it can be determined that P300 has an effect on the lactylation level of the specific protein.

[0026] Step S102: If it is determined that there is an influence of the lactylation level, the influence information of the lactylation level on the intramyocardial hemorrhage injury is determined by adding an experimental subject to an expression level regulator.

[0027] In this embodiment, an experimental subject to which an expression regulator is added is used for the experiment. By conducting experiments and testing on the experimental subject, the effect of the lactylation level of P300-regulated specific proteins, i.e., key proteins, on intramyocardial hemorrhage injury can be determined. For example, the intramyocardial hemorrhage injury here can be ST-segment elevation myocardial infarction STEMI reperfusion intramyocardial hemorrhage injury.

[0028] Optionally, the expression level regulator may be an inhibitor, and the information on the influence of the lactylation level on intramyocardial hemorrhage injury is determined by using an experimental subject to which the expression level regulator is added, including: establishing a STEMI reperfusion intramyocardial hemorrhage model of the experimental subject; adding the inhibitor to the model, and performing immunohistochemistry experiments and tests based on the model to which the inhibitor is added to determine the myocardial injury index information of the experimental subject, wherein the injury image information includes the myocardial injury index information.

[0029] For example, if the experimental subject is a mouse, 30 C57BL / 6J-WT mice (8 weeks, 18-24g) were selected and divided into a sham operation group, a STEMI reperfusion myocardial hemorrhage group, and a STEMI reperfusion myocardial hemorrhage + p300 inhibitor group, with 10 mice in each group. A 7.0T magnetic resonance system was used, with a mouse-specific coil and a small animal-specific model 1030II ECG gating, and gadopentetate dimeglumine injection was used as a contrast agent. After the mice were killed, heart tissue was taken for testing. a. HE staining was used to evaluate the morphological changes of mice. b. TTC staining was used to evaluate the range of myocardial infarction. c. Masson staining was used to evaluate the level of myocardial fibrosis in mice. d. Immunohistochemistry and Western Blot experiments were used to evaluate myocardial injury-related indicators and the expression levels of p300 and key proteins. e. Electron microscopy was used to observe the ultrastructure of mouse cardiomyocytes. f. Co-IP experiments were used to detect the binding strength of p300 and key proteins in heart tissue and the lactylation level of key proteins.

[0030] This embodiment can provide a method for determining whether P300 has an effect on intramyocardial hemorrhage damage. By determining whether P300 has an effect on the lactylation level of myocardial tissue, the effect on intramyocardial hemorrhage damage can be determined.

[0031] In some optional implementations of any of the embodiments of the present disclosure, determining whether the P300 affects the lactylation level of the specific protein comprises: if a lactylation modification site regulated by lactyl transferase is determined to exist in the peripheral boundary zone of the infarct zone in the myocardial tissue, determining whether the P300 affects the lactylation level of the specific protein.

[0032] Among these optional implementations, in order to further clarify the regulatory mechanism, this study attempts to find the lactoacyl transferase of key proteins. Given that Sirtuin family proteins are important lactoacyl transferases, this study intends to select Sirtuin family enzymes (SIRT1-7) as lactoacyl transferases. SIRT1-7 and key protein plasmids were constructed and transfected into HL-1 mouse cardiomyocytes. Co-IP and Pan-Kla Co-IP experiments were used to detect the interaction between lactoacyl transferase and key proteins and its effect on lactylation levels.

[0033] Furthermore, the key protein lactylation sites regulated by p300 can be identified: key protein-WT, key protein-lactylation site mutant plasmids and p300, deacetylase plasmids were constructed and transfected into HL-1 mouse cardiomyocytes respectively. The key protein lactylation sites regulated by p300 were determined using Pan-Kla Co-IP experiments.

[0034] Optionally, the determining the presence of a lactylation modification site regulated by lactyl transferase comprises: using a lactylation modification material to screen whether the specific protein in the surrounding boundary zone has a lactylation modification site to obtain a screening result; performing mass spectrometry analysis on the co-precipitation results of P300 and the protein of the myocardial tissue in the surrounding boundary zone to determine the specific protein that interacts with the P300, and determining the lactylation modification site regulated by the P300 through the screening results and the results of the mass spectrometry analysis.

[0035] The above-mentioned execution subject can take protein samples from the peripheral border area of ​​the infarct area in the myocardial tissue, add p300 antibodies and Protein A / G beads to the protein samples, and obtain co-precipitated proteins. The co-precipitated proteins are separated by SDS-PAGE electrophoresis to obtain protein gel. The protein separation bands on the gel are stained with a dye to visualize the proteins. The protein gel blocks are then enzymatically hydrolyzed into peptides and subjected to mass spectrometry analysis to screen out proteins that interact with p300 as specific proteins.

[0036] After screening specific proteins, cross-analysis of the lactylation modification results and mass spectrometry combined results can be performed to identify the key protein lactylation sites regulated by p300 in the infarct boundary zone.

[0037] like Figure 2 As shown, a flow chart for determining the lactylation modification sites regulated by the P300 is shown.

[0038] Optionally, the above determination of the presence of a lactylation modification site regulated by lactyl transferase may include: obtaining a precipitation result of lactylation immunoprecipitation using cells of myocardial tissue; and determining the presence of a lactylation modification site regulated by the P300 based on the precipitation result.

[0039] The lactylated modified material includes: plasmids for transfecting mouse cardiomyocytes: a first experimental group plasmid and a second experimental group plasmid, wherein the first experimental group plasmid includes: p300-full-length plasmid and p300-inactivated mutant plasmid; the second experimental group plasmid includes: si-control plasmid and si-p300 plasmid.

[0040] The above execution entities can clarify the lactylation modification effect of p300 on key proteins: a. Construct p300-full-length and p300-inactive mutant plasmids, and transfect HL-1 mouse cardiomyocytes respectively. b. Construct si-Control and si-p300, and transfect HL-1 mouse cardiomyocytes respectively. c. Treat HL-1 mouse cardiomyocytes with p300 inhibitors. In the above grouping, the lactylation immunoprecipitation (Pan-Kla Co-IP) experiment was used to detect the lactylation modification effect of p300 on key proteins.

[0041] like Figure 3a As shown, the figure shows the molecular mechanism of p300 lactylation modification of key proteins in the border zone of STEMI reperfusion myocardial hemorrhage.

[0042] In some optional implementations of any embodiment of the present disclosure, the method further includes: knocking out a gene corresponding to at least one target domain of the P300 to obtain at least one plasmid connected to the knockout result; transfecting the at least one plasmid into the myocardial tissue cells of the experimental subject to determine the interaction between the P300 and the specific protein, and the interaction domain in the P300.

[0043] The at least one plasmid includes: p300-TAZ1-Delete domain plasmid, p300-KIX-Delete domain plasmid, p300-HAT-Delete domain plasmid, p300-TAZ2-Delete domain plasmid, key protein-full length plasmid, key protein-Delete domain plasmid.

[0044] In these optional implementations, the interaction and interaction domains between p300 and key proteins can be clarified: construct plasmids of p300-full length, p300-TAZ1-Delete domain, p300-KIX-Delete domain, p300-HAT-Delete domain, p300-TAZ2-Delete domain, key protein-full length and key protein-domain Delete, and transfect HL-1 mouse cardiomyocytes respectively. Confocal co-localization, PLA fluorescence in situ gene protein analysis, and Co-IP experiments are used to determine the interaction and interaction domains between p300 and key proteins. Specifically, the p300-TAZ1-Delete domain refers to the knockout of the TAZ1 plasmid in p300.

[0045] In some optional implementations of any embodiment of the present disclosure, the expression level regulator is an inhibitor, and the influence information of the lactylation level on intramyocardial hemorrhage injury is determined by using an experimental subject to which the expression level regulator is added, including: establishing a STEMI reperfusion intramyocardial hemorrhage model of the experimental subject; adding the inhibitor to the model, and performing immunohistochemistry experiments and tests based on the model to which the inhibitor is added to determine the myocardial injury index information of the experimental subject, and the influence information includes the myocardial injury index information.

[0046] In these implementations, a mouse STEMI reperfusion intramyocardial hemorrhage model can be prepared: the mouse is anesthetized by intraperitoneal injection of 1% sodium pentobarbital (50 mg / kg), the oral tracheal intubation is connected to the small animal respiratory anesthesia machine, the mouse is fixed in a supine position on a circulating heating operating table, and the limbs are connected to the small animal standard lead electrodes. The skin of the mouse chest surgical area is prepared and disinfected, the skin is cut along the 3rd and 4th intercostal spaces on the left side of the sternum, and the subcutaneous tissue and muscle are bluntly separated layer by layer to fully expose the heart. The left anterior descending coronary artery (LAD) is identified under a microscope, and a suture needle with a thread is used to penetrate the myocardial surface LAD at 2 to 3 mm below the lower edge of the left atrial appendage. The LAD is then ligated and the myocardial tissue of the left ventricular anterior wall gradually turns white. The electrocardiogram shows that the ST segment continues to be arched and elevated, indicating that ischemia is successful. After ischemia, the ligature is loosened to allow blood flow to reperfuse, the myocardial color of the ischemic area is restored, the subcutaneous tissue and muscle are sutured layer by layer, and finally the chest cavity is closed. After the mice recovered spontaneous breathing, the endotracheal tube was removed and they were placed on a 37.5°C warming pad and placed in a cage after they recovered the ability to crawl automatically. Mice in the sham operation group only underwent thoracotomy without ligation.

[0047] Afterwards, the changes in myocardial injury in mice after the action of p300 inhibitors can be evaluated: 30 C57BL / 6J-WT mice (8 weeks, 18-24g) were selected and divided into a sham operation group, a STEMI reperfusion myocardial hemorrhage group, and a STEMI reperfusion myocardial hemorrhage + p300 inhibitor group, with 10 mice in each group. A 7.0T magnetic resonance system was used, with a mouse-specific coil and a small animal-specific model 1030II ECG gating, and gadopentetate dimeglumine injection was used as a contrast agent. After the mice were killed, heart tissue was taken for testing. a. HE staining was used to evaluate the morphological changes in mice. b. TTC staining was used to evaluate the range of myocardial infarction. c. Masson staining was used to evaluate the level of myocardial fibrosis in mice. d. Immunohistochemistry and Western Blot experiments were used to evaluate myocardial injury-related indicators and the expression levels of p300 and key proteins. e. Electron microscopy was used to observe the ultrastructure of mouse cardiomyocytes. f. Co-IP experiment was used to detect the binding strength of p300 and key proteins in cardiac tissue and the acylation level of key proteins.

[0048] like Figure 3b Shown is a flow chart showing the role of p300 regulatory key protein lactylation modification in STEMI reperfusion myocardial hemorrhage injury.

[0049] In addition, mice with myocardial-specific key protein lactylation site mutations can also be constructed. 20 C57BL / 6J-WT mice and 20 C57BL / 6J-point mutant mice were selected, and the above two types of mice were used to create a reperfusion myocardial hemorrhage model. A 7.0T magnetic resonance system and a professional coil were used to detect the mouse heart. The heart tissue was taken after the mice were killed for detection. HE staining, TTC staining, Masson staining, immunohistochemistry, Western Blot and transmission electron microscopy were used to evaluate the heart damage of mice. Co-IP experiments were used to detect the level of key protein lactylation in heart tissue.

[0050] like Figure 3c Shown is a flow chart showing the role of key protein lactylation modifications in STEMI reperfusion intramyocardial hemorrhage injury.

[0051] The present disclosure provides a device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury, which is used to perform the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury described in the above embodiment, such as Figure 4As shown, the device includes: a first determination unit, configured to determine whether P300 has an effect on the lactylation level of the specific protein if the specific protein acted on by P300 exists in the myocardial tissue; a second determination unit, configured to determine the influence information of the lactylation level on the intramyocardial hemorrhage injury by adding an expression regulator to the experimental subject if it is determined that there is an effect on the lactylation level.

[0052] The device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage damage provided in the above-mentioned embodiment of the present disclosure and the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage damage provided in the embodiment of the present disclosure are based on the same inventive concept and have the same beneficial effects as the methods adopted, run or implemented by the application programs stored therein.

[0053] The disclosed embodiment also provides an electronic device corresponding to the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury provided in the aforementioned embodiment, so as to execute the aforementioned method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury. The disclosed embodiment is not limited thereto.

[0054] Please refer to Figure 5 , which shows a schematic diagram of an electronic device provided by some embodiments of the present disclosure. Figure 5 As shown, the electronic device 50 includes: a processor 500, a memory 501, a bus 502 and a communication interface 503, and the processor 500, the communication interface 503 and the memory 501 are connected via the bus 502; the memory 501 stores a computer program that can be run on the processor 500, and the processor 500 executes the method provided in any of the aforementioned embodiments of the present disclosure when running the computer program.

[0055] The memory 501 may include a high-speed random access memory (RAM), and may also include a non-volatile memory, such as at least one disk storage. The communication connection between the system network element and at least one other network element is realized through at least one communication interface 503 (which may be wired or wireless), and the Internet, wide area network, local area network, metropolitan area network, etc. may be used.

[0056] The bus 502 may be an ISA bus, a PCI bus, or an EISA bus, etc. The bus may be divided into an address bus, a data bus, a control bus, etc. The memory 501 is used to store a program, and the processor 500 executes the program after receiving an execution instruction. The method for determining the effect of the targeted acyltransferase P300 on intramyocardial hemorrhage injury disclosed in any embodiment of the aforementioned embodiment of the present disclosure may be applied to the processor 500, or implemented by the processor 500.

[0057] The processor 500 may be an integrated circuit chip with signal processing capabilities. In the implementation process, each step of the above method can be completed by the hardware integrated logic circuit in the processor 500 or the instruction in the form of software. The above processor 500 can be a general-purpose processor, including a central processing unit (CPU), a network processor (NP), etc.; it can also be a digital signal processor (DSP), an application-specific integrated circuit (ASIC), a field-programmable gate array (FPGA) or other programmable logic devices, discrete gates or transistor logic devices, discrete hardware components. The methods, steps and logic block diagrams disclosed in the embodiments of the present disclosure can be implemented or executed. The general-purpose processor can be a microprocessor or the processor can also be any conventional processor. The steps of the method disclosed in conjunction with the embodiments of the present disclosure can be directly embodied as a hardware decoding processor to be executed, or the hardware and software modules in the decoding processor can be executed. The software module can be located in a mature storage medium in the field such as a random access memory, a flash memory, a read-only memory, a programmable read-only memory or an electrically erasable programmable memory, a register, etc. The storage medium is located in the memory 501, and the processor 500 reads the information in the memory 501 and completes the steps of the above method in combination with its hardware.

[0058] The electronic device provided by the embodiment of the present disclosure and the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury provided by the embodiment of the present disclosure are based on the same inventive concept and have the same beneficial effects as the methods adopted, operated or implemented therein.

[0059] The present disclosure also provides a computer-readable storage medium corresponding to the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury provided in the above embodiment. Figure 6 The computer-readable storage medium shown is a CD 60 on which a computer program (i.e., a program product) is stored. When the computer program is executed by a processor, the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury provided in any of the aforementioned embodiments will be executed.

[0060] It should be noted that examples of the computer-readable storage medium may also include, but are not limited to, phase change memory (PRAM), static random access memory (SRAM), dynamic random access memory (DRAM), other types of random access memory (RAM), read-only memory (ROM), electrically erasable programmable read-only memory (EEPROM), flash memory or other optical or magnetic storage media, which are not listed here one by one.

[0061] The computer-readable storage medium provided in the above-mentioned embodiment of the present disclosure and the method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury provided in the embodiment of the present disclosure are based on the same inventive concept and have the same beneficial effects as the method adopted, run or implemented by the application program stored therein.

[0062] It should be noted that:

[0063] In the above text, the term "comprises", "comprising" or any other variant thereof is intended to cover non-exclusive inclusion, so that a process, method, article or device including a series of elements includes not only those elements, but also other elements not explicitly listed, or also includes elements inherent to such process, method, article or device. In the absence of further restrictions, an element defined by the sentence "comprising a ..." does not exclude the presence of other identical elements in the process, method, article or device including the element. In addition, it should be noted that the scope of the method and device in the embodiments of the present disclosure is not limited to performing functions in the order shown or discussed, and may also include performing functions in a substantially simultaneous manner or in reverse order according to the functions involved, for example, the described method may be performed in an order different from that described, and various steps may also be added, omitted, or combined. In addition, the features described with reference to certain examples may be combined in other examples.

[0064] Through the description of the above implementation methods, those skilled in the art can clearly understand that the above-mentioned embodiment methods can be implemented by means of software plus a necessary general hardware platform, and of course by hardware, but in many cases the former is a better implementation method. Based on such an understanding, the technical solution of the present disclosure, or the part that contributes to the prior art, can be embodied in the form of a software product, which is stored in a storage medium (such as ROM / RAM, a magnetic disk, or an optical disk), and includes a number of instructions for enabling a terminal (which can be a mobile phone, a computer, a server, an air conditioner, or a network device, etc.) to execute the methods described in each embodiment of the present disclosure.

[0065] The embodiments of the present disclosure are described above in conjunction with the accompanying drawings, which are only specific implementation modes of the present disclosure. However, the present disclosure is not limited to the above-mentioned specific implementation modes. The above-mentioned specific implementation modes are merely illustrative and not restrictive. Under the guidance of the present disclosure, ordinary technicians in this field can also make many forms without departing from the purpose of the present disclosure and the scope of protection of the claims, all of which are within the protection of the present disclosure.

Claims

1. A method for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury, characterized in that: include: If the specific protein acted by P300 exists in the myocardial tissue, determining whether the P300 has an effect on the lactylation level of the specific protein; If it is determined that there is an effect of the lactylation level, the effect of the lactylation level on intramyocardial hemorrhage damage is determined by adding an expression level regulator to the experimental subject.

2. The method according to claim 1, characterized in that Determining the effect of the P300 on whether the specific protein has a lactylation level comprises: If the lactylation modification site regulated by lactyl transferase is determined to exist in the border area around the infarct zone in the myocardial tissue, it is determined whether the P300 affects the lactylation level of the specific protein.

3. The method according to claim 2, characterized in that The determination of the presence of a lactoylation modification site regulated by lactoacyl transferase comprises: Using the lactylated modified material, screening whether the specific protein in the surrounding border region has a lactylated modified effect, and obtaining a screening result; The immunoprecipitation results are determined by P300 and the proteins of the myocardial tissue in the surrounding border zone, and the immunoprecipitation results are subjected to mass spectrometry analysis to determine the specific proteins that interact with the P300, and the lactylation modification sites regulated by the P300 are determined through the screening results and the results of the mass spectrometry analysis.

4. The method according to claim 3, characterized in that The lactylated modified material comprises: Plasmids used for transfecting mouse cardiomyocytes: plasmids of the first experimental group and plasmids of the second experimental group, wherein the plasmids of the first experimental group include: p300-full-length plasmid and p300-inactivated mutant plasmid; the plasmids of the second experimental group include: si-control plasmid and si-p300 plasmid.

5. The method according to claim 2, characterized in that: The determination of the presence of a lactoylation modification site regulated by lactoacyl transferase comprises: Obtain the precipitation results of lactylated immunoprecipitation using cells from myocardial tissue; According to the precipitation results, it is determined that there is a lactylation modification site regulated by the P300.

6. The method according to claim 1, characterized in that The method further comprises: Knocking out a gene corresponding to at least one target domain of the P300 to obtain at least one plasmid connected with the knockout result; The at least one plasmid is transfected into the myocardial tissue cells of the experimental subject to determine the interaction between the P300 and the specific protein, and the interaction domain in the P300.

7. The method according to claim 6, characterized in that The at least one plasmid includes: p300-TAZ1-Delete domain plasmid, p300-KIX-Delete domain plasmid, p300-HAT-Delete domain plasmid, p300-TAZ2-Delete domain plasmid, key protein-full length plasmid, key protein-Delete domain plasmid.

8. The method according to claim 1, characterized in that Determining the effect of the P300 on whether the specific protein has a lactylation level comprises: Through the target modification site, constructing the gene plasmid corresponding to lactacyl transferase and the gene plasmid of the specific protein; transfecting the gene plasmid corresponding to lactacyl transferase and the gene plasmid of the specific protein into the myocardial tissue cells of the experimental subject to regulate the specific protein of the myocardial tissue cells; The transfected myocardial tissue cells are tested to determine whether the P300 has an effect on the lactylation level of the specific protein.

9. The method according to claim 1, characterized in that: The expression regulator is an inhibitor, and the information on the effect of the lactylation level on intramyocardial hemorrhage injury is determined by adding the expression regulator to the experimental subject, including: Establishing a STEMI reperfusion intramyocardial hemorrhage model in the experimental subject; The inhibitor is added to the model, and based on the model with the inhibitor added, immunohistochemistry experiments and tests are performed to determine the myocardial injury index information of the experimental subject, wherein the impact information includes the myocardial injury index information.

10. A device for determining the effect of targeted acyltransferase P300 on intramyocardial hemorrhage injury, characterized in that: include: A first determination unit is configured to determine whether P300 has an effect on the lactylation level of a specific protein if the specific protein acted on by P300 exists in the myocardial tissue; The second determination unit is configured to determine the influence of the lactylation level on the intramyocardial hemorrhage injury by adding the experimental subject to the expression level regulator if it is determined that there is an influence of the lactylation level.

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