Detection system and therapeutic agent for endometriosis

Abstract

The invention discloses an endometriosis detection system and a therapeutic agent, and belongs to the technical field of biomedical engineering.The detection system comprises an acquisition module and a prediction module, the acquisition module is used for acquiring clinical indexes, and the clinical indexes comprise CCL21; and the prediction module is used for predicting the probability of endometriosis through the prediction model and the clinical indexes. The therapeutic agent includes an inhibitor of CCL21. By detecting the expression level of CCL21 in the body of a patient and combining related biomarkers, the disease progress and the treatment effect can be more accurately predicted, so that an individualized treatment scheme is formulated; the CCL21 inhibitor provides accurate and effective targeted therapy, and provides possibility for individualized therapy and early intervention.

Description

Technical Field

[0001] The present invention relates to the technical field of biomedical engineering, and in particular to a detection system and a therapeutic agent for endometriosis. Background Art

[0002] Endometriosis, also known as endometriosis, is a common gynecological disease in which the endometrium (containing glands and stroma) grows outside the uterine cavity. The cause of this disease has not yet been fully clarified, but it is believed that it may be related to the body's immune function, genetic factors, and environmental factors.

[0003] The main treatments for endometriosis include medication (such as hormone drugs) and surgery. These treatments have significant disadvantages: although hormone therapy can relieve symptoms, it lacks sufficient specificity, and long-term use may cause hormone imbalance, leading to side effects such as weight gain, mood swings, and decreased bone density. Although surgical treatment can remove ectopic tissue, it has a high risk of surgery, cannot cure the disease, and has a high recurrence rate after surgery.

[0004] Therefore, it is necessary to develop a detection system and therapeutic agent for endometriosis to detect and intervene in endometriosis at the molecular mechanism. Summary of the invention

[0005] In view of the above technical problems existing in the prior art, the present invention provides a detection system and a therapeutic agent for endometriosis to avoid the systemic side effects caused by hormone therapy.

[0006] The present invention provides a detection system for endometriosis, comprising a collection module and a prediction module, wherein the collection module is used to collect clinical indicators, wherein the clinical indicators include CCL21; and the prediction module is used to predict the probability of endometriosis through a prediction model and clinical indicators.

[0007] Preferably, the detection system further comprises a training module, wherein the training module is used to train the prediction model.

[0008] Methods for training predictive models include:

[0009] Collecting test data, wherein the test data includes index values ​​of clinical indicators;

[0010] Based on the machine learning method, the prediction model is obtained by training with the detection data.

[0011] Preferably, the clinical indicators further include ACKR1 and CFD;

[0012] The machine learning includes random forest or logistic regression.

[0013] The second aspect of the present invention also provides a therapeutic agent for endometriosis, comprising an inhibitor of CCL21.

[0014] Preferably, the inhibitor is selected from a first inhibitor, a second inhibitor and a third inhibitor;

[0015] The interfering RNA sequences of the first inhibitor include: Seq ID NO.1 and Seq ID NO.2;

[0016] The interfering RNA sequences of the second inhibitor include: Seq ID NO.3 and Seq ID NO.4;

[0017] The interfering RNA sequences of the third inhibitor include: Seq ID NO.5 and Seq ID NO.6.

[0018] Preferably, the therapeutic agent further comprises a carrier and an excipient; the therapeutic agent is a mixture of a carrier, an inhibitor and an excipient.

[0019] Preferably, the carrier is selected from liposomes, nanomicelles, nanoemulsions and polymer nanoparticles;

[0020] The polymer nanoparticles include poly(lactic-co-glycolic acid).

[0021] Preferably, the administration of the therapeutic agent includes injection or topical application.

[0022] Preferably, the therapeutic agent is used to treat endometriosis.

[0023] Compared with the prior art, the beneficial effect of the present invention is that by detecting the expression level of CCL21 in the patient and combining it with its related biomarkers, the progression of the disease and the treatment effect can be more accurately predicted, thereby formulating an individualized treatment plan. BRIEF DESCRIPTION OF THE DRAWINGS

[0024] Figure 1 It is a comparison chart of the up-regulation of CCL21 in multiple data sets;

[0025] Figure 2 It is the ROC curve of the data set;

[0026] Figure 3 This is the Western blot test image of normal tissue and endometriosis tissue;

[0027] Figure 4 This is the immunofluorescence staining of normal tissue and endometriosis tissue;

[0028] Figure 5 This is the RT-qPCR analysis of normal tissue and endometriosis tissue;

[0029] Figure 6 This is a comparison chart of RT-qPCR of siRNA silencing;

[0030] Figure 7 This is a Western blot detection image of siRNA silencing;

[0031] Figure 8 is a representative image of immunofluorescence staining of siRNA silencing;

[0032] Fig. 9 This is the migration test diagram of siRNA silencing;

[0033] Fig.10 This is the invasion test diagram of siRNA silencing;

[0034] Fig.11 are representative images of immunofluorescence staining of Ki67 and PCNA silenced by siRNA;

[0035] Fig.12 It is a representative picture of apoptosis;

[0036] Fig.13 It is a logic block diagram of the detection system of the present invention. DETAILED DESCRIPTION

[0037] In order to make the purpose, technical solution and advantages of the embodiments of the present invention clearer, the technical solution in the embodiments of the present invention will be clearly and completely described below in conjunction with the drawings in the embodiments of the present invention. Obviously, the described embodiments are part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without creative work are within the scope of protection of the present invention.

[0038] The present invention is further described in detail below in conjunction with the accompanying drawings:

[0039] Although current treatments can alleviate symptoms to a certain extent, most treatments fail to effectively prevent the progression of the disease, and symptoms even recur after drug withdrawal. This means that existing treatments fail to fundamentally control the pathological process, and patients often require long-term treatment, resulting in a decline in quality of life.

[0040] Most existing treatment options focus on suppressing symptoms, and usually only start intervention when the disease symptoms are obvious, missing the important opportunity for intervention in the early stage of the disease and failing to effectively prevent further deterioration of the disease. The persistent inflammatory response that causes the disease to worsen is not effectively controlled, which in turn leads to the inability to effectively curb the pathological process.

[0041] Current drug treatments fail to accurately target the molecular pathological mechanisms of endometriosis, resulting in limited efficacy and significant side effects. The pathogenesis of endometriosis is complex, involving multiple aspects such as the immune system, inflammatory response, and hormone regulation, and existing treatment options often only relieve symptoms without fundamentally intervening in the molecular mechanisms of the disease.

[0042] In view of the shortcomings of existing treatment methods, the present invention studies the key role of CCL21 (chemokine ligand 21) in endometriosis and proposes an endometriosis detection system and therapeutic agent based on CCL21. By targeting CCL21 and its related NF-κB signaling pathway, it is expected to more accurately intervene in the pathological process of endometriosis and avoid the systemic side effects caused by hormone therapy.

[0043] Most current treatment options rely on symptom assessment and clinical experience, and lack accurate prediction tools for individual patients' conditions. Therefore, the treatment effect varies from patient to patient, and individualized treatment cannot be achieved. Most existing detection / diagnosis options are based on the patient's clinical manifestations and imaging examinations, ignoring the differences in molecular markers in the patient's body, resulting in the inability to accurately adjust the treatment plan based on individual differences. There is currently no reliable prediction tool based on molecular mechanisms, and it is impossible to provide patients with accurate treatment plans.

[0044] The first aspect of the present invention provides a detection system for endometriosis, such as Fig.13 , comprising a collection module 1 and a prediction module 2, wherein the collection module is used to collect the index value of the biomarker;

[0045] The prediction model is used to predict the probability of suffering from endometriosis through the indicator value and the prediction model.

[0046] The detection system further includes a training module 3, which is used to train the prediction model. The specific training method includes:

[0047] Collecting test data, wherein the test data includes an indicator value of a biomarker;

[0048] Based on the machine learning method, the prediction model is obtained by training with the detection data.

[0049] Among them, the biomarkers include CCL21, atypical chemokine receptor 1 (ACKR1), human complement factor D (CFD), and other clinical indicators, such as CA125; the machine learning methods include random forest, logistic regression, etc., but are not limited to these.

[0050] By constructing a prediction model based on CCL21 and its related inflammatory factors, a theoretical basis is provided for the personalized treatment of endometriosis. By detecting the expression level of CCL21 in patients and combining it with related biomarkers, the progression of the disease and the treatment effect can be predicted more accurately, thereby formulating a personalized treatment plan. It provides clinicians with effective diagnostic tools to help achieve early diagnosis and personalized treatment.

[0051] To investigate the importance of CCL21 in the development of endometriosis, we detected its gene expression in multiple datasets. Figure 1 Compared with the control group, the CCL21-related mRNA level in the endometriosis group was continuously upregulated in the following multiple data sets: GSE5108, GSE11691, GSE23339 and GSE25628, among which GSE (Gene Expression Omnibus Series) represents a data set composed of a series of related samples. GSE enables researchers to view and analyze data under the entire experimental design framework and understand the comparisons and experimental results between different samples (GSM).

[0052] like Figure 2 The ROC curve results showed that CCL21 had a good diagnostic value for endometriosis. The AUC of the GEE5108 dataset was 0.9256, P was 0.0007; the AUC of the GSE11691 dataset was 0.7901, P was 0.038; the AUC of the GSE23339 dataset was 0.8556, P was 0.009; the AUC of the GSE25628 dataset was 0.8958, P was 0.0051. The horizontal axis was specificity (1-Specificity) and the vertical axis was sensitivity (Sensitivity).

[0053] As shown in Table 1, in the transcriptome sequencing RNA-seq data, the expression of CCL21, ACKR1 (atypical chemokine receptor 1), and CFD (human complement factor D) in endometriosis tissues was high compared with normal tissues.

[0054] Table 1

[0055]

[0056] like Figure 3 , Figure 4 and Figure 5 , Western blot, immunofluorescence staining, and RT-qPCR analysis revealed that CCL21 expression was elevated in ectopic lesions of endometriosis patients and mice. Figure 3In the table, β-Actin (β-actin) was used as a reference; Figure 4 The scale bar is 100 μm. The results showed that CCL21, as an important inflammation-related gene, was upregulated in endometriosis lesions and was closely related to the occurrence and progression of endometriosis.

[0057] The second aspect of the present invention provides a therapeutic agent for endometriosis, including an interfering RNA (siRNA) of CCL21. In order to clarify the relationship between CCL21 and endometriosis, in a test, the CCL21 gene was silenced in 12Z cells (ectopic endometrial glandular epithelial cells). Specific CCL21 siRNA sequences were designed for different regions of the CCL21 open reading frame, see Table 2, to evaluate the knockdown efficiency of CCL21.

[0058] Table 2

[0059]

[0060] Among the three siRNA constructs tested, Figure 6 and Figure 7 siRNA-3 (217-237) was the most effective in inhibiting CCL21 expression. 12Z cells were used as the control group, and 12Z cells after siRNA silencing were used as the silencing group. Therefore, siRNA-3 (217-237) was selected to knock down the expression of CCL21 for subsequent experiments. Figure 8 , Immunofluorescence staining showed that the expression of CCL21 in the silencing group (si-CCL21) was downregulated compared with the control group, the scale bar is 100μm. In addition, Fig. 9 The cell CCL21 was knocked down, and then the wound healing experiment was performed; the Transwell method was used to determine the invasion ability of the control cells and si-CCL21 cells. Fig.10 , which can significantly inhibit the migration and invasion of 12Z cells. Fig.11 and Fig.12 , siRNA can promote the apoptosis rate of 12Z cells.

[0061] The shortcomings of the existing technologies in the treatment of endometriosis include lack of specific treatment, limited treatment effect and lack of accurate prediction tools. These shortcomings are mainly due to the failure of current treatment methods to accurately intervene in pathological mechanisms, lack of early treatment plans and failure to achieve individualized treatment. The present invention is expected to solve these problems by targeting CCL21 and its related molecular pathways, provide an accurate and effective targeted treatment method, and provide possibilities for individualized treatment and early intervention.

[0062] The present invention aims to solve the following key problems in the current treatment of endometriosis:

[0063] Existing treatments lack specificity and efficiency: Currently, most treatments for endometriosis are to control symptoms through medication (such as hormone therapy) or to remove ectopic lesions through surgery. Although these treatments can relieve symptoms, the effects are usually temporary and accompanied by significant side effects. Existing treatments cannot accurately target pathological mechanisms, and long-term use may lead to a decrease in the patient's quality of life.

[0064] Failure to effectively inhibit pathological progression and recurrence: Existing treatments have failed to fundamentally control the pathological progression of endometriosis, especially in the early stages of pathological changes, and treatment is usually difficult to effectively prevent further deterioration of the disease. Although medication and surgery can relieve symptoms, they are often accompanied by a high recurrence rate, and patients need to receive repeated treatments.

[0065] Lack of accurate molecular markers and predictive tools: Current treatments often lack accurate diagnostic and predictive tools, making it impossible to develop individualized treatment plans based on individual differences among patients. The treatment effects vary from patient to patient, and there is a lack of systematic, molecular-mechanism-based clinical decision-making basis.

[0066] Lack of innovative treatment strategies targeting pathological mechanisms: The pathogenesis of endometriosis involves complex immune and inflammatory responses, among which the role of CCL21 in this process has not been fully understood. Existing treatments have failed to effectively intervene in these molecular pathological mechanisms.

[0067] The present invention can achieve the following goals by targeting CCL21 and its related signaling pathways:

[0068] Providing targeted treatment: By targeting CCL21 and its related NF-κB signaling pathway, the present invention can accurately intervene in the inflammatory response and immune response of endometriosis, fundamentally slowing down or inhibiting the pathological progression. The treatment effect will be more precise and reduce the side effects of traditional hormone therapy.

[0069] Effectively slowing down the progression and recurrence of the disease: The treatment method of the present invention can effectively inhibit the pathological progression of endometriosis, reduce the proliferation, migration and invasive growth of endometriosis tissue, and reduce the probability of disease recurrence. By inhibiting the inflammatory response and inhibiting the activation of the NF-κB signaling pathway, the present invention can fundamentally control the expansion of the lesion and delay or prevent the recurrence of the disease.

[0070] Personalized treatment: By developing molecular markers and predictive models based on CCL21, we can provide each patient with accurate diagnostic tools and achieve personalized treatment. According to the expression level of CCL21 in the patient's body and related molecular characteristics, a more accurate treatment plan can be formulated to improve the treatment effect and reduce unnecessary side effects.

[0071] Improve the quality of life of patients: Through the treatment scheme targeting CCL21, the present invention can not only effectively control the pathological progression of endometriosis, but also significantly reduce the occurrence of side effects, thereby improving the quality of life of patients. The long-term effect of treatment is more stable, reducing the patient's dependence on repeated treatment.

[0072] Innovative treatment methods: This invention provides a new molecular target by revealing the promoting role of CCL21 in endometriosis, which is expected to become an innovative treatment strategy for endometriosis and provide a new treatment direction for clinical treatment.

[0073] The invention should meet the following performance indicators:

[0074] Therapeutic effect: The therapeutic method of the present invention should be able to effectively inhibit the inflammatory response of endometriosis, the proliferation, migration and invasive growth of endometriotic tissue, reduce the area of ​​lesion tissue, alleviate pathological progression, and delay or prevent recurrence.

[0075] Minimizing side effects: This treatment method should be able to significantly reduce the side effects of traditional hormone therapy, such as weight gain, mood swings, and decreased bone density, to ensure the safety of patients.

[0076] Diagnostic accuracy: Molecular marker detection tools based on CCL21 should have high diagnostic accuracy (such as sensitivity and specificity), be able to detect endometriosis at an early stage, and provide a decision-making basis for individualized treatment.

[0077] Personalized treatment: Based on the CCL21 expression level and other related molecular characteristics, individualized treatment plans can be provided for different patients, and dynamically adjusted according to the patient's treatment response.

[0078] Clinical applicability: The treatment plan should be able to be used conveniently and quickly in clinical practice, and can significantly improve the clinical efficacy and quality of life of patients.

[0079] The present invention is committed to providing a precise, effective and low-side effect treatment method for endometriosis by targeting CCL21 and its related NF-κB signaling pathway. Through early intervention, reduction of pathological progression and recurrence, and combining molecular markers and predictive models, it provides clinicians with individualized treatment plans, ultimately improving the quality of life of patients and promoting the innovative development of endometriosis treatment.

[0080] The therapeutic agent of the present invention includes an interfering RNA of CCL21, which is used to target and inhibit the activity of CCL21. More specifically, the interfering RNA includes: a first inhibitor siRNA-1, a second inhibitor siRNA-2, and a third inhibitor siRNA-3. Among them, the sequence of siRNA-1 includes Seq ID NO.1 and Seq ID NO.2; the sequence of siRNA-2 includes Seq ID NO.3 and Seq ID NO.4; the sequence of siRNA-3 includes: Seq ID NO.5 and Seq ID NO.6.

[0081] The concentration range of CCL21 targeted inhibitors can be adjusted as needed, usually within the range of 1-10 mg / ml. The specific concentration should be determined based on the expression level of CCL21 in the patient, the efficacy requirements and the results of clinical trials.

[0082] The therapeutic agent of the present invention targets CCL21 and its related signaling pathways, can accurately intervene in the molecular mechanism of endometriosis, and effectively inhibit the pathological process. Compared with traditional hormone therapy, the present invention has stronger targeting, less side effects, and more lasting therapeutic effect. Traditional treatment methods are often accompanied by large side effects, such as weight gain, decreased bone density, etc., while the present invention significantly reduces the impact on other systems of the body by targeting specific molecular targets. Clinical trial results show that the recurrence rate of this treatment method is lower than that of traditional treatment methods, and symptoms can be effectively controlled. By providing a molecular marker detection tool based on CCL21, early diagnosis of the disease can be achieved, and an individualized treatment plan can be formulated according to the specific pathological characteristics of the patient. Individualized treatment can significantly improve the treatment effect and reduce unnecessary drug use, thereby reducing patient discomfort and treatment costs. Repeated treatment and long-term use of drugs in traditional treatment plans can be reduced, thereby reducing the overall treatment cost of patients. In addition, the drug formula and production process are simplified, the operation is convenient, and it is convenient for clinical promotion and application. It can effectively inhibit the pathological process of endometriosis and significantly improve the treatment efficiency. Compared with traditional treatment methods, the efficacy of the present invention is faster and more stable, and the quality of life of patients is significantly improved. The present invention provides a new targeted treatment scheme based on CCL21 and its related NF-κB signaling pathway, which has high clinical application prospects. This treatment method can not only provide a new treatment strategy, but also provide a new direction for the early diagnosis and treatment monitoring of endometriosis.

[0083] The therapeutic agent of the present invention is characterized by high efficiency, precision and safety. By targeting CCL21 and its related molecular pathways, the pathological progression of endometriosis can be fundamentally inhibited, side effects can be reduced, disease recurrence can be controlled, and a more individualized treatment plan can be provided for patients. In addition, the treatment method of the present invention is simple and easy to implement, can effectively improve treatment efficiency, and reduce treatment costs, and provides an innovative and promising solution for the clinical treatment of endometriosis.

[0084] Example 1

[0085] CCL21 targeting inhibitor siRNA-3, with a concentration of 5 mg / ml, was produced by genetic engineering methods. Liposomes were used as delivery carriers. The main component of liposomes was lecithin, which has good biocompatibility and drug carrying capacity. Stabilizers such as mannitol (2%) and surfactants (such as PEG-5000) were added to enhance the solubility and stability of the drug.

[0086] The ratio of siRNA-3 to liposome is 1:5, that is, 1 mg of CCL21 inhibitor corresponds to 5 mg of liposome carrier.

[0087] The preparation method comprises:

[0088] Step 101: Inhibitor synthesis and purification. The CCL21 inhibitor is produced by genetic recombination technology, purified by affinity chromatography to obtain a high-purity inhibitor, and finally dissolved to an appropriate concentration.

[0089] Step 102: Prepare liposomes.

[0090] Phosphatidylcholine and cholesterol are mixed and dissolved in an organic solvent, and liposomes are prepared by thin film hydration method; after the solvent evaporates, the lipid film is rehydrated with water phase and converted into liposome particles, which are crushed by ultrasonic wave to reach a particle size of 100-200nm. Liposome carriers can also use nanomicelles or nanoemulsions. These carriers can provide different drug release characteristics, such as longer half-life or stronger intracellular delivery ability. Different delivery carriers can be selected according to the properties of the drug and clinical needs.

[0091] During the preparation of liposomes, the stability of liposomes and the release rate of drugs can be affected by adjusting the ratio of lecithin to cholesterol (e.g., 1:1 to 1:2). The most appropriate ratio can be determined through experimental optimization.

[0092] Step 103: Mixing the inhibitor with the liposome. The inhibitor and the liposome suspension are fully mixed at room temperature to obtain the final therapeutic agent 1. After mixing, it needs to be freeze-dried to prepare a freeze-dried powder for storage.

[0093] Example 2

[0094] The preparation method comprises:

[0095] Step 201: Inhibitor synthesis. Prepare a small molecule CCL21 inhibitor with high affinity by chemical synthesis. Ensure that the inhibitor has high affinity and can specifically bind to CCL21.

[0096] Step 202: Sanction the carrier.

[0097] Polymer nanoparticles (such as poly(lactic-co-glycolic acid) PLGA) are used for drug delivery. PLGA has good biodegradability and is suitable for sustained-release drug delivery.

[0098] Other auxiliary ingredients: phosphate buffer, antioxidants (such as vitamin E), etc.

[0099] PLGA nanoparticles can be prepared by double emulsion solvent evaporation method. PLGA and drugs are dissolved in a solvent, and the solvent is removed after forming an emulsion to finally obtain drug-loaded nanoparticles.

[0100] Step 203: The inhibitor is mixed with the carrier to obtain therapeutic agent 2.

[0101] The ratio of CCL21 small molecule inhibitor to polymer nanoparticles is 1:10, that is, 1 mg of inhibitor corresponds to 10 mg of nanoparticles. The CCL21 small molecule inhibitor is mixed with PLGA nanoparticles to ensure that the inhibitor is evenly distributed and can be released stably. The particle size and drug loading of the particles are optimized by adjusting the molecular weight and emulsification process of PLGA.

[0102] The drug release behavior of nanoparticles can be optimized by adjusting the ratio of the molecular weight of PLGA to a water-soluble polymer (such as PEG) to make it more in line with clinical treatment needs.

[0103] The therapeutic agent of the present invention can be administered not only by intravenous injection, but also by local application (such as intrauterine injection or intraperitoneal injection) to increase the concentration of the drug in the target tissue. The administration method can be flexibly selected according to the patient's condition, the severity of the disease and clinical feedback.

[0104] Administration method 1: injection.

[0105] The steps for drug administration are as follows:

[0106] Step 301: Dissolution of therapeutic agent.

[0107] The lyophilized CCL21 inhibitor is re-dissolved with the liposome carrier or nanoparticle carrier and mixed thoroughly to obtain an injection solution. The solvent used should be sterile phosphate buffer, and the dissolution process should be carried out at room temperature (20-25°C) to ensure that the drug is completely dissolved.

[0108] Step 302: administer the injection solution by intravenous injection or local injection.

[0109] The recommended dose is 1 mg / kg per injection, and the treatment cycle is once a week for 4 consecutive weeks.

[0110] Step 303: Clinical observation and adjustment.

[0111] During the treatment, the concentration of CCL21 inhibitors in the patient's body and the clinical response of the drug (such as symptom improvement, changes in pathological tissue, etc.) should be monitored regularly. The dosage and frequency of administration can be adjusted according to the patient's treatment response.

[0112] Method of administration 2: topical application with enhanced drug penetration.

[0113] The steps for drug administration are as follows:

[0114] Step 501: Applying the therapeutic agent: Applying the therapeutic agent to the ectopic lesion area of ​​the uterus or abdominal cavity.

[0115] The therapeutic agent can be prepared as an application agent in the form of a nanoparticle solution or a liposome emulsion before application to increase the penetration of the drug at the lesion site.

[0116] Step 502: Accelerate penetration.

[0117] It can be combined with ultrasonic treatment equipment to accelerate the drug penetration process and increase the local concentration of the drug through the auxiliary effect of ultrasound. The frequency of ultrasound should be set to 1-3MHz and irradiated for 5-10 minutes.

[0118] The speed and duration of drug release are key factors affecting the therapeutic effect. The present invention can optimize the release behavior of the drug and achieve sustained and stable drug release by adjusting the properties of the carrier material (such as the molecular weight of PLGA, the membrane composition of the liposome, etc.). Different release modes can be selected according to clinical needs, such as fast release, sustained release or controlled release.

[0119] Through these specific embodiments, the present invention can flexibly select different drug formulations and dosing regimens according to treatment needs, achieve precise targeted therapy, significantly improve the therapeutic effect of endometriosis, and reduce side effects through an optimized drug delivery system. These embodiments can effectively solve the problems of lack of precise targeted therapy and large drug side effects in the prior art, and provide an efficient, safe and personalized treatment method for clinical practice.

[0120] The present invention inhibits CCL21, thereby controlling the inflammatory response and preventing the further development of the pathological process. The treatment by targeting CCL21 can not only effectively inhibit the proliferation and migration of ectopic endometrial cells, but also slow down the inflammatory response of the diseased tissue, thereby controlling the progression of the disease.

[0121] Through early treatment of CCL21, it is expected to play a therapeutic role in the early stage of pathological changes, thereby effectively controlling the progression of the disease. The present invention regulates the NF-κB signaling pathway and inhibits the release of downstream inflammatory factors, thereby reducing the inflammatory response and achieving the effect of alleviating symptoms.

[0122] The above are only preferred embodiments of the present invention and are not intended to limit the present invention. For those skilled in the art, the present invention may have various modifications and variations. Any modification, equivalent replacement, improvement, etc. made within the spirit and principle of the present invention shall be included in the protection scope of the present invention.

Claims

1. A system for detecting endometriosis, characterized in that: Including acquisition module and prediction module, The acquisition module is used to collect clinical indicators, and the clinical indicators include CCL21; The prediction module is used to predict the probability of endometriosis through a prediction model and clinical indicators.

2. The detection system according to claim 1, characterized in that: It also includes a training module, wherein the training module is used to train the prediction model. Methods for training predictive models include: Collecting test data, wherein the test data includes index values ​​of clinical indicators; Based on the machine learning method, the prediction model is obtained by training with the detection data.

3. The detection system according to claim 2, characterized in that: The clinical indicators also include ACKR1 and CFD.

4. The detection system according to claim 3, characterized in that: The machine learning includes random forest or logistic regression.

5. A therapeutic agent for endometriosis, characterized in that: Including inhibitors of CCL21.

6. The therapeutic agent according to claim 5, characterized in that The inhibitor is selected from a first inhibitor, a second inhibitor, and a third inhibitor; The interfering RNA sequences of the first inhibitor include: Seq ID NO.1 and Seq ID NO.2; The interfering RNA sequences of the second inhibitor include: Seq ID NO.3 and Seq ID NO.4; The interfering RNA sequences of the third inhibitor include: Seq ID NO.5 and Seq ID NO.

6.

7. The therapeutic agent according to claim 5, characterized in that It also includes carriers and excipients; The therapeutic agent is a mixture of carrier, inhibitor and excipient.

8. The therapeutic agent according to claim 7, characterized in that The carrier is selected from liposomes, nanomicelles, nanoemulsions and polymer nanoparticles; The auxiliary materials include phosphate buffer and antioxidant; The polymer nanoparticles include poly(lactic-co-glycolic acid).

9. The therapeutic agent according to claim 5, characterized in that The administration of the therapeutic agent includes injection or local application.

10. The therapeutic agent according to any one of claims 5 to 9, characterized in that Used to treat endometriosis.

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