Detection system and therapeutic agent for endometriosis

Abstract

The present invention discloses a detection system and therapeutic agent for endometriosis, belonging to the field of biomedical engineering technology. The detection system includes an acquisition module and a prediction module. The acquisition module is used to collect clinical indicators, including CCL21; the prediction module is used to predict the probability of endometriosis using a prediction model and clinical indicators. The therapeutic agent includes a CCL21 inhibitor. By detecting the expression level of CCL21 in a patient and combining it with its related biomarkers, the progression of the disease and the treatment effect can be more accurately predicted, thereby formulating a personalized treatment plan. CCL21 inhibitors provide precise and effective targeted therapy and open up the possibility of personalized treatment 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 therapeutic agent for endometriosis. Background Art

[0002] Endometriosis, also known as endometriosis, is a common gynecological condition in which the endometrium (containing glands and stroma) grows outside the uterine cavity. While the cause of this condition is not fully understood, it is believed to be related to the body's immune system, genetic factors, and environmental factors.

[0003] The main treatments for endometriosis include medications (such as hormones) and surgery. These treatments have significant drawbacks. For example, while hormone therapy can alleviate symptoms, it lacks specificity, and long-term use can cause hormone imbalances, leading to side effects such as weight gain, mood swings, and decreased bone density. While surgery can remove the endometriosis, it carries significant risks, is incurable, and has a high recurrence rate.

[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 level. 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 an acquisition module and a prediction module. The acquisition module is used to acquire clinical indicators, including CCL21; the prediction module is used to predict the probability of endometriosis based on 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 a machine learning method, a 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 further 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 existing technology, the beneficial effect of the present invention is that by detecting the expression level of CCL21 in the patient's body 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 This is a comparison chart of the up-regulation of CCL21 in multiple datasets;

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

[0026] Figure 3 This is a 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] Figure 9 This is the migration test graph of siRNA silencing;

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

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

[0035] Figure 12 It is a representative diagram of cell apoptosis;

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

[0037] To make the objectives, technical solutions, and advantages of the embodiments of the present invention more clear, the technical solutions in the embodiments of the present invention will be clearly and completely described below in conjunction with the accompanying 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 making creative efforts shall fall within the scope of protection of the present invention.

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

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

[0040] Existing treatment options mostly focus on suppressing symptoms, often only beginning intervention when symptoms become apparent. This misses the crucial opportunity for intervention early in the disease process and fails to effectively prevent further progression. The persistent inflammatory response that worsens the disease is also not effectively controlled, leading to an inability to effectively curb the pathological process.

[0041] Current drug treatments fail to precisely target the molecular pathogenesis of endometriosis, resulting in limited efficacy and significant side effects. The pathogenesis of endometriosis is complex, involving multiple factors, including the immune system, inflammatory response, and hormonal regulation. Existing treatments often only alleviate symptoms without fundamentally addressing the disease's molecular mechanisms.

[0042] In response to the shortcomings of existing treatment methods, the present invention studies the key role of CCL21 (chemokine ligand 21) in endometriosis and proposes a CCL21-based endometriosis detection system and therapeutic agent. 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, lacking precise predictive tools tailored to individual patient conditions. Consequently, treatment outcomes vary from patient to patient, making personalized treatment impossible. Existing testing / diagnostic protocols are mostly based on clinical manifestations and imaging studies, ignoring differences in molecular markers across patients. This results in treatment plans being unable to be precisely tailored to individual differences. Currently, there are no reliable predictive tools based on molecular mechanisms, making it impossible to provide patients with precise treatment plans.

[0044] The first aspect of the present invention provides a detection system for endometriosis, such as Figure 13 , comprising an acquisition module 1 and a prediction module 2, wherein the acquisition module is used to acquire 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 index values ​​of biomarkers;

[0048] Based on a machine learning method, a 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 thereto.

[0050] By constructing a predictive model based on CCL21 and its related inflammatory factors, a theoretical basis is provided for personalized treatment of endometriosis. By measuring CCL21 expression levels in patients and combining it with related biomarkers, disease progression and treatment efficacy can be more accurately predicted, leading to the development of personalized treatment plans. This provides clinicians with an effective diagnostic tool, enabling early diagnosis and personalized treatment.

[0051] To investigate the importance of CCL21 in the development of endometriosis, we examined its gene expression in multiple datasets. Figure 1 Compared with the control group, the CCL21-related mRNA level (Relative mRNA level) of the endometriosis group was consistently upregulated in the following multiple datasets: GSE5108, GSE11691, GSE23339 and GSE25628. Among them, GSE (Gene Expression Omnibus Series) represents a dataset 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; and the AUC of the GSE25628 dataset was 0.8958, P was 0.0051. The horizontal axis is specificity (1-Specificity) and the vertical axis is 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 higher than that in normal tissues.

[0054] Table 1

[0055]

[0056] like Figure 3 、 Figure 4 and Figure 5 , Western blot, immunofluorescence staining, and RT-qPCR analysis found 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, is upregulated in endometriosis lesions and is closely related to the occurrence and progression of endometriosis.

[0057] A second aspect of the present invention provides therapeutic agents for endometriosis, including interfering RNA (siRNA) against CCL21. To clarify the relationship between CCL21 and endometriosis, in one test, the CCL21 gene was silenced in 12Z cells (ectopic endometrial glandular epithelial cells). Specific CCL21 siRNA sequences were designed targeting different regions of the CCL21 open reading frame (see Table 2) to assess 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 silenced 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, Figure 9 The cell CCL21 was knocked down, and then the wound healing experiment was performed; the invasion ability of the control cells and si-CCL21 cells was determined by Transwell method. Figure 10 , which can significantly inhibit the migration and invasion of 12Z cells. Figure 11 and Figure 12 , siRNA can promote the apoptosis rate of 12Z cells.

[0061] Existing treatments for endometriosis suffer from shortcomings such as a lack of specificity, limited efficacy, and a dearth of accurate predictive tools. These shortcomings stem primarily from the inability of current treatments to precisely intervene in pathological mechanisms, the lack of early treatment options, and the inability to personalize treatment. The present invention, by targeting CCL21 and its associated molecular pathways, promises to address these issues, providing a precise and effective targeted therapy and potentially enabling personalized 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 effectiveness: Currently, most treatments for endometriosis involve controlling symptoms with medications (such as hormone therapy) or surgically removing endometriotic lesions. While these treatments can alleviate symptoms, the effects are often temporary and accompanied by significant side effects. Existing treatments cannot precisely target the pathological mechanisms, and long-term use may result in a decrease in patients' quality of life.

[0064] Failure to effectively inhibit pathological progression and recurrence: Existing treatments fail to fundamentally control the pathological progression of endometriosis, especially in the early stages of pathological changes. Treatment is often ineffective in preventing further deterioration of the disease. Although medications and surgery can alleviate symptoms, they are often accompanied by high recurrence rates, requiring patients to undergo 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 patient differences. 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 therapeutic strategies targeting pathological mechanisms: The pathogenesis of endometriosis involves complex immune and inflammatory responses, and the role of CCL21 in this process is not fully understood. Existing treatments fail to effectively intervene in these molecular pathological mechanisms.

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

[0068] Providing targeted treatment: By targeting CCL21 and its associated NF-κB signaling pathway, this invention can precisely intervene in the inflammatory and immune responses of endometriosis, fundamentally slowing or inhibiting pathological progression. This will result in more precise treatment effects and reduce the side effects of traditional hormone therapy.

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

[0070] Personalized treatment: By developing molecular markers and predictive models based on CCL21, we can provide each patient with precise diagnostic tools and personalized treatment. Based on the patient's CCL21 expression level and related molecular characteristics, more precise treatment plans can be formulated, improving treatment efficacy and reducing unnecessary side effects.

[0071] Improved patient quality of life: By targeting CCL21, this treatment not only effectively controls the pathological progression of endometriosis but also significantly reduces the occurrence of side effects, thereby improving patients' quality of life. The long-term effects of treatment are more stable, reducing patients' reliance on repeated treatments.

[0072] Innovative treatment method: This invention reveals the promoting role of CCL21 in endometriosis and provides a new molecular target. It 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 treatment 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 patient safety.

[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 in the early stages, and provide a decision-making basis for personalized treatment.

[0077] Personalized treatment: Based on CCL21 expression levels and other related molecular characteristics, personalized 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 easy and quick to apply in clinical practice, and significantly improve the clinical efficacy and quality of life of patients.

[0079] By targeting CCL21 and its associated NF-κB signaling pathway, this invention aims to provide a precise, effective, and low-side effect treatment for endometriosis. By enabling early intervention, reducing pathological progression and recurrence, and combining molecular markers with predictive models, this approach provides clinicians with personalized treatment options, ultimately improving patients' quality of life and driving innovative development in endometriosis treatment.

[0080] The therapeutic agents of the present invention include interfering RNAs (RNAs) targeting CCL21 for inhibiting CCL21 activity. Specifically, the interfering RNAs include: a first inhibitor, siRNA-1; a second inhibitor, siRNA-2; and a third inhibitor, siRNA-3. The sequence of siRNA-1 includes Seq ID Nos. 1 and 2; the sequence of siRNA-2 includes Seq ID Nos. 3 and 4; and the sequence of siRNA-3 includes Seq ID Nos. 5 and 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 associated signaling pathways, precisely intervening in the molecular mechanisms of endometriosis and effectively inhibiting the pathological progression. Compared with traditional hormone therapies, the present invention offers stronger targeting, fewer side effects, and more sustained therapeutic effects. Traditional treatments are often associated with significant side effects, such as weight gain and decreased bone density. However, by targeting specific molecular targets, the present invention significantly reduces the impact on other body systems. Clinical trial results show that this treatment method has a lower recurrence rate than traditional treatments and effectively controls symptoms. By providing a molecular marker detection tool based on CCL21, early diagnosis of the disease can be achieved, allowing for personalized treatment plans tailored to the patient's specific pathological features. Personalized treatment can significantly improve therapeutic efficacy and reduce unnecessary medication use, thereby reducing patient discomfort and treatment costs. It can also reduce the repeated treatments and long-term medication use associated with traditional treatments, thereby lowering overall treatment costs. Furthermore, the simplified drug formulation and production process facilitate easy operation, facilitating clinical application. It effectively inhibits the pathological progression of endometriosis and significantly improves treatment efficiency. Compared with traditional treatments, the present invention offers faster and more stable efficacy, significantly improving patients' quality of life. This invention provides a novel targeted therapy based on CCL21 and its associated NF-κB signaling pathway, with promising clinical applications. This treatment approach not only offers a new therapeutic strategy but also provides a new direction for early diagnosis and treatment monitoring of endometriosis.

[0083] The therapeutic agent of the present invention is highly effective, precise, and safe. By targeting CCL21 and its associated molecular pathways, it can fundamentally inhibit the pathological progression of endometriosis, reduce side effects, control disease recurrence, and provide patients with a more personalized treatment plan. Furthermore, the treatment method of the present invention is simple and easy to implement, effectively improving treatment efficiency and reducing treatment costs, providing an innovative and promising solution for the clinical treatment of endometriosis.

[0084] Example 1

[0085] The CCL21-targeting inhibitor siRNA-3, produced via genetic engineering at a concentration of 5 mg / ml, uses liposomes as a delivery vehicle. The primary component of liposomes is phosphatidylcholine, which has excellent biocompatibility and drug-carrying capacity. Stabilizers such as mannitol (2%) and surfactants (e.g., PEG-5000) are added to enhance drug solubility and stability.

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

[0087] The preparation method comprises:

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

[0089] Step 102: Prepare liposomes.

[0090] Liposomes are prepared by dissolving a mixture of lecithin and cholesterol in an organic solvent using a thin film hydration method. After evaporation of the solvent, the lipid film is rehydrated with water and converted into liposome particles, which are then disrupted by ultrasound to a particle size of 100-200 nm. Liposome carriers can also be nanomicelles or nanoemulsions. These carriers can provide different drug release characteristics, such as a longer half-life or enhanced intracellular delivery. Different delivery carriers can be selected based on the properties of the drug and clinical needs.

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

[0092] Step 103: Mixing the inhibitor with the liposomes. The inhibitor and liposome suspension are thoroughly mixed at room temperature to obtain the final therapeutic agent 1. After mixing, the mixture needs to be freeze-dried to form 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) copolymer (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 using the double emulsion solvent evaporation method. PLGA and the drug are dissolved in a solvent, and after forming an emulsion, the solvent is removed to obtain drug-loaded nanoparticles.

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

[0101] The ratio of the CCL21 small molecule inhibitor to polymer nanoparticles was 1:10, meaning 1 mg of inhibitor corresponded to 10 mg of nanoparticles. The CCL21 small molecule inhibitor was mixed with PLGA nanoparticles to ensure uniform distribution and stable release of the inhibitor. The particle size and drug loading were optimized by adjusting the PLGA molecular weight and emulsification process.

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

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

[0104] Method of administration: injection.

[0105] The steps for administration are as follows:

[0106] Step 301: Dissolution of therapeutic agent.

[0107] Redissolve the lyophilized CCL21 inhibitor in the liposome carrier or nanoparticle carrier and mix thoroughly to obtain an injection solution. The solvent used should be sterile phosphate buffered saline. The dissolution process should be performed at room temperature (20-25°C) to ensure complete dissolution of the drug.

[0108] Step 302: administer the injection solution intravenously or locally.

[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 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] Second route of administration: topical application and enhanced drug penetration.

[0113] The steps for administration are as follows:

[0114] Step 501: Applying a therapeutic agent: Applying a therapeutic agent to the uterus or the ectopic lesion area of ​​the 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] Ultrasonic therapy can be combined with ultrasound therapy 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 the irradiation should be continuous for 5-10 minutes.

[0118] The rate and duration of drug release are key factors influencing therapeutic efficacy. By adjusting the properties of the carrier material (e.g., the molecular weight of PLGA, the membrane composition of the liposome, etc.), the present invention can optimize drug release behavior and achieve sustained and stable drug release. Depending on clinical needs, different release modes can be selected, such as rapid release, sustained release, or controlled release.

[0119] Through these specific embodiments, the present invention enables flexible selection of different drug formulations and dosing regimens based on treatment needs, achieving precise targeted therapy, significantly improving the therapeutic efficacy of endometriosis, and reducing side effects through an optimized drug delivery system. These embodiments effectively address the problems of the existing technology, such as the lack of precise targeted therapy and significant drug side effects, providing a highly efficient, safe, and personalized treatment approach for clinical practice.

[0120] The present invention inhibits CCL21, thereby controlling the inflammatory response and preventing further progression of the pathological process. Targeting CCL21 not only effectively inhibits the proliferation and migration of ectopic endometrial cells, but also slows the inflammatory response of the diseased tissue, thereby controlling the progression of the disease.

[0121] Early treatment targeting CCL21 is expected to have therapeutic effects at the early stages of pathological changes, thereby effectively controlling the progression of the disease. This 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 merely preferred embodiments of the present invention and are not intended to limit the present invention. Those skilled in the art will readily appreciate that various modifications and variations of the present invention are possible. Any modifications, equivalent substitutions, or improvements made within the spirit and principles of the present invention shall be included within the scope of protection 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; the clinical indicators also include ACKR1 and CFD; Also includes a training module, 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 a machine learning method, a prediction model is obtained by training with the detection data.

2. The detection system according to claim 1, characterized in that The machine learning includes random forest or logistic regression.

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