99 results about "Ferroptosis" patented technology

This invention discloses a multi-target synergistic anti-liver cancer medical food granule and its preparation method. The granule uses medicinal and edible homologous foods and novel resource foods as raw materials, and is composed of curcumin extract, esterified fat-soluble EGCG, Moringa leaf powder, yeast β-glucan, Astragalus extract, Schisandra extract, Salvia miltiorrhiza extract, Poria cocos powder, resistant dextrin, and erythritol in a specific ratio to construct a three-dimensional synergistic system of "direct killing-immune regulation-liver protection," which can induce ferroptosis in liver cancer cells, inhibit protective autophagy, activate the body's immunity, and protect liver cells. This invention employs directional extraction, multi-layer coating, and high-pressure fusion granulation technology. Nanoparticle liposome encapsulation, esterification modification, and pH-responsive enteric coating improve the stability and bioavailability of the components, solving the problems of poor water solubility, low absorption, and easy degradation of natural active ingredients. The granule has clear efficacy, high safety, and stable process, and can be used as a medical food for adjuvant therapy and nutritional support during the recovery period of liver cancer.

The application discloses a new use of Leonurine or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating radiation-induced brain injury, specifically, providing a safe and effective therapeutic drug for iron death, neuroinflammation, neuron damage and lipid metabolism disorder accompanying the radiation-induced brain injury, solving the technical problem of lack of specific treatment means in the prior art, and having a wide clinical application prospect. Experiments adopt a C57BL / c mouse 30 Gy whole brain X-ray radiation model, and results show that Leonurine can significantly improve the body weight decrease and survival rate of the model mice, reduce the serum IL-6 and IFN-alpha levels, inhibit the activation of microglial cells in the cerebral cortex and hippocampus, protect and repair damaged neurons, and improve the ultrastructure of mitochondria and synapses; meanwhile, the expression of GPX4 and SLC7A11 proteins in the brain tissue is up-regulated, the GSH content is increased to inhibit iron death, and the levels of GPE, GPS and GPC related to lipid metabolism are restored.

This invention discloses a method for constructing a prognostic model for acute myeloid leukemia (AML) based on ferroptosis-related genes. The method involves acquiring gene expression data from AML patients and healthy samples to screen for differentially expressed ferroptosis-related genes (DEGs) associated with AML. Using univariate Cox proportional hazards regression analysis, LASSO regression analysis, and multivariate Cox proportional hazards regression analysis, key genes ACSF2, SLC7A11, DNAJB6, and SOCS1 are selected from these DEGs. A prognostic risk model is constructed based on the expression levels of these key genes and their corresponding multivariate Cox regression coefficients. The risk score formula is: Risk Score = 0.534 × ACSF2 expression value - 0.453 × DNAJB6 expression value + 0.194 × SLC7A11 expression value + 0.308 × SOCS1 expression value. The prognostic model constructed in this invention has high predictive accuracy and reliability, effectively stratifying the risk and assessing the prognosis of AML patients, providing an important reference for the clinical treatment of AML.

The present invention relates to a medium composition for in vitro fertilization and / or in vitro culture comprising a compound represented by chemical formula 1 or a pharmaceutically acceptable salt thereof, and a method using same. The compound or composition suppresses reactive oxygen species and lipid peroxidation in ovarian granulosa cells to preventing cytotoxicity and mitochondrial dysfunction caused by apoptosis and ferroptosis, leading to an improvement in the quality of aged oocytes, and to increase the developmental rate and blastocyst formation rate of pre-implantation embryos, thereby improving the efficiency of in vitro fertilization. In addition, treatment with the medium composition during the vitrification process of in vitro–fertilized embryos improves re-expansion and survival rates, thereby reducing structural and metabolic damage. Accordingly, the present invention can be advantageously applied to an assisted reproductive technology for treating infertility and subfertility, and in vitro fertilization and / or in vitro culture for improving the propagation efficiency of livestock.

This invention discloses a ferroptosis target identification system and method based on an attention mechanism, belonging to the field of artificial intelligence technology. The system includes modules for extracting multi-source features of ferroptosis regulation, labeling weak signal targets, calculating attention potential energy mapping, and ranking ferroptosis targets. It extracts multimodal features from transcriptome expression, molecular interaction networks, and ferroptosis pathway annotations. Targets with expression intensities below a preset threshold that participate in the ferroptosis pathway are labeled with weak signals. Weak signal characteristics are injected, and a potential energy bias is constructed to complete attention potential energy mapping. Then, through pathway mapping and cross-pathway linkage identification and fusion weights, the target linkage degree is calculated and ranked. This system solves the problem of traditional methods easily neglecting weak signal targets, and can identify targets with insignificant expression changes in the ferroptosis regulatory network. Through attention and pathway-level linkage modeling, the comprehensiveness of target identification is improved, and the obtained ranking results have stability and discriminative power, making it suitable for the identification and research of ferroptosis-related targets.

This invention proposes the application of psoralen as an Nrf2 agonist in drug preparation. This invention is the first to discover that psoralen is a specific Nrf2 agonist. Psoralen can directly target and bind to the Nrf2 protein, improving its stability, promoting its phosphorylation and nuclear translocation, thereby activating the Nrf2 signaling pathway, upregulating the expression of downstream antioxidant, anti-inflammatory, and anti-ferroptosis-related proteins, and achieving cell protection and tissue repair functions.

The present invention aims to provide a cytoprotective agent against ferroptosis that contains DHMBA as an active ingredient, by verifying the effect of DHMBA in suppressing ferroptotic cell death using DN model mice and human renal tubular cells HK-2, for each useful agent containing DHMBA as an active ingredient. [Solution] The present invention provides a cell agent for ferroptosis that has a cytoprotective effect against ferroptosis, comprising 3,5-dihydroxy-4-methoxybenzyl alcohol as an active ingredient.

The application belongs to the technical field of biological medicine, and particularly relates to application of long-chain non-coding RNA expression inhibition in esophageal cancer ferroptosis inducer sensitization. The application first reveals dynamic change of long-chain non-coding RNA ENSG00000250658 in esophageal squamous cell carcinoma metastasis based on single-cell sequencing data, detects expression of ENSG00000250658 in esophageal squamous cell carcinoma tissue and correlation with prognosis by using LNA probe-based RNA in-situ hybridization technology, and first finds that knocking down ENSG00000250658 can increase killing effect of ferroptosis inducer on esophageal squamous cell carcinoma cells. Therefore, the application provides a new technical scheme and thought for clinical diagnosis and treatment of esophageal cancer.

The application relates to the technical field of biological medicine, and discloses a targeted ferroptosis-inducing conjugate as well as a preparation method and application thereof. The structural formula of the conjugate is as follows: the conjugate contains a prostate cancer targeting peptide segment WHDGFK, and is connected with an iron death-inducing antibacterial peptide KRIVKWIIKLLR through a disulfide bond, so that the conjugate has tumor targeting and microenvironment response release functions, not only endows the antibacterial peptide KRIVKWIIKLLR with tumor selective delivery capacity, but also realizes specific release of the active peptide in target cells by reducing the disulfide bond by using high-concentration glutathione (GSH) in tumor cells, thereby synergistically enhancing the antitumor effect and reducing the systemic toxicity.

The application provides a copper-nitroimidazole complex which is self-assembled by coordination of copper ions and 2-nitroimidazole. The complex only contains copper ions and 2-nitroimidazole, and the simple two-component combination can realize the chemical kinetics treatment of GSH metabolism enhancement and induce iron death. The copper-nitroimidazole complex has GSH response and hypoxia responsiveness as a nanodrug, and can selectively act in tumor cells. The nanodrug releases copper ions and 2-nitroimidazole in tumor cells, 2-nitroimidazole consumes NADPH under hypoxic conditions to hinder the synthesis of GSH, and copper ions also consume GSH. The consumption of GSH enhances the Cu 2+ / Cu + mediated Fenton reaction to produce active oxygen. 2-nitroimidazole and copper ions self-assemble to form a nanodrug, which greatly improves the loading capacity of 2-nitroimidazole.

The application discloses a 4-oxoquinoline derivative with ferroptosis inhibiting activity and a preparation method and application thereof, and belongs to the technical field of medicines. The application provides a compound shown in general formula I or a pharmaceutically acceptable salt, isomer, polymorph, or pharmaceutically acceptable solvate thereof, which has the effect of inhibiting ferroptosis, and further treating and / or preventing renal fibrosis, thereby providing a new scheme for treating and / or preventing renal fibrosis. The application provides application of the compound shown in general formula I or the pharmaceutically acceptable salt, isomer, polymorph, or pharmaceutically acceptable solvate thereof in preparation of a ferroptosis inhibitor and in preparation of a medicine for treating and / or preventing renal fibrosis, and the application field of the compound shown in general formula I or the pharmaceutically acceptable salt, isomer, polymorph, or pharmaceutically acceptable solvate thereof is expanded.

This invention relates to the field of congenital heart disease treatment technology, and discloses the application of sapropterin in the prevention and treatment of bisphenol fluorene-induced congenital heart disease in fetuses. The congenital heart disease includes cardiac structural defects, heart failure, or cardiomyocyte lesions, specifically selected from ventricular septal defects, atrial septal defects, tetralogy of Fallot, myocardial hypertrophy, decreased cardiac ejection fraction, decreased short-axis contraction rate, cardiomyocyte ferroptosis, myocardial tissue inflammatory infiltration, or myocardial collagen fibrosis. Sapropterin is used as a direct supplement to biological tetrahydropterin (BH4). Through exogenous intervention, it precisely reverses the endogenous BH4 deficiency caused by bisphenol fluorene exposure, restores the expression of GTP cyclase 1 (GCH1) and the dynamic balance of RNA m6A, and upregulates the level of YTH domain family protein 2 (YTHDF2), thereby blocking ferroptosis signal transduction, reducing oxidative stress and inflammatory response, and inhibiting the process of myocardial tissue fibrosis at the molecular level.

The application provides application of glutaroyl-CoA dehydrogenase in inducing ferroptosis of liver cancer cells, and belongs to the technical field of biotechnology.The application provides application of glutaroyl-CoA dehydrogenase (GCDH) in preparing products for evaluating risk of liver cancer and evaluating prognosis risk of liver cancer, and the tumor stage and T grade can be estimated by detecting the expression amount of GCDH, and the survival effect of liver cancer patients is evaluated.The application provides application of the overexpression reagent of GCDH in preparing products for inhibiting proliferation of liver cancer cells and inducing ferroptosis of liver cancer cells, and the ferroptosis of liver cancer cells is promoted by overexpressing GCDH in cells, and the colony formation ability of liver cancer cells is reduced.Further, the application provides application of the overexpression reagent of GCDH combined with a CA9 inhibitor in preparing products for inhibiting proliferation of liver cancer cells.

This invention discloses the application of a "Super Brain-Boosting Capsule," belonging to the field of pharmaceutical technology. The Super Brain-Boosting Capsule is used in the preparation of drugs for treating Alzheimer's disease. The capsule enhances the mitochondrial membrane potential of Glu-treated HT22 cells by inhibiting ferroptosis. At the transcriptional level, the capsule activates the expression of key Nrf2 / HO-1 / GPX4 signaling molecules NRF2, HO-1, GPX4, SLC7A11, ACSL4, FTH1, and FPN1, while reversing the expression of Bcl-2, Caspase-3, and Caspase-9 to inhibit apoptosis in AD cells. This invention reveals that the Super Brain-Boosting Capsule, based on the Nrf2 / HO-1 / GPX4 pathway, inhibits Glu-induced ferroptosis in HT22 cells, which can treat Alzheimer's disease. This invention provides experimental evidence and direction for the further development of the Super Brain-Boosting Capsule in the prevention and treatment of Alzheimer's disease and other neurodegenerative diseases.

A small molecule composition, comprising licochalcone A, licochalcone C, licochalcone D, licochalcone E, echinatin, isoliquiritigenin, formononetin, liquiritigenin, licoflavone C, glabrol, licoisoflavone A and licoisoflavone B, and the use thereof in preparing anticancer or antitumor drugs, anti-ferroptosis drugs, or drugs for sensitization of anticancer or antitumor drugs. The small molecule composition can also be used in combination with other antitumor drugs.

This invention relates to the field of biopharmaceutical technology, and in particular to the application of myrotoxin A in the preparation of drugs for treating prostate cancer. This invention is the first to discover the function of myrotoxin A in inducing ferroptosis in DU145 prostate cancer cells by targeting and inhibiting ACSL3 protein, and its inhibitory effect on prostate cancer proliferation. Specific embodiments of this invention reveal for the first time that myrotoxin A can precisely utilize the unique metabolic vulnerability of prostate cancer cells, significantly downregulating the expression of ACSL3 protein in DU145 cells at the protein level. This, in turn, by relieving the inhibition of ferroptosis by ACSL3 protein, specifically induces ferroptosis in prostate cancer cells, ultimately effectively inhibiting tumor cell growth and achieving the therapeutic goal of targeting prostate cancer development.

This invention belongs to the field of pharmaceutical technology and relates to a composite nanoparticle that synergistically induces ferroptosis and antitumor immune responses, as well as its preparation method. The invention first provides a dihydroartemisinin dimer prodrug or a pharmaceutically acceptable salt thereof with the following structure. Then, composite nanoparticles are prepared using the aforementioned dihydroartemisinin dimer prodrug or its pharmaceutically acceptable salt as the main drug component. The composite nanoparticles are prepared by covalently binding an albumin-manganese dioxide complex and ferritin, while simultaneously co-encapsulating the dihydroartemisinin dimer prodrug or its pharmaceutically acceptable salt and a photosensitizer. The composite nanoparticles prepared by this invention can disrupt the reducing homeostasis of tumor cells by simultaneously enhancing ROS generation and GSH consumption. PDT and CDT synergistically enhance ROS generation, and manganese dioxide can also promote GSH consumption. These composite nanoparticles can significantly improve drug targeting and significantly enhance antitumor activity.

The application discloses a double-drug self-enhanced layered double hydroxide nanosystem and application thereof. The iron-ruthenium layered double hydroxide in the nanosystem has double enzyme activity, can efficiently catalyze H2O2 to generate O2 and active oxygen in a tumor microenvironment, significantly relieves hypoxia while inducing oxidative stress, the MCT4 specific inhibitor VB124 in the system creates an acidic microenvironment by blocking lactic acid output, amplifies the catalytic efficiency of FeRu, and establishes a self-enhanced catalytic effect; and the co-loaded epigenetic regulator JQ1 down-regulates the expression of PD-L1 by inhibiting BET protein. The system amplifies the catalytic efficiency of FeRu, significantly induces ferroptosis, reverses the immunosuppressive microenvironment with the help of epigenetic regulation, induces the release of damage-associated molecular patterns, causes the infiltration of immune cells, and finally cooperatively triggers a strong anti-tumor immune response. The self-enhanced catalysis-epigenetic regulation synergistic strategy realized by the system provides an innovative solution for improving the effect of tumor immunotherapy.

This invention relates to a pH-responsive multifunctional nanoplatform M@FNPs, a drug-loaded composition MP@FNPs, its preparation method, and its applications, belonging to the fields of nanomaterials and biomedical materials technology. The preparation method of the pH-responsive multifunctional nanoplatform M@FNPs includes the following steps: in-situ doping of ZIF-8 with ferric ions during synthesis to obtain iron-doped ZIF-8; dissolving magnesium peroxide nanoparticles and iron-doped ZIF-8 in a solvent; ultrasonicating to load the magnesium peroxide nanoparticles onto the iron-doped ZIF-8; and drying to obtain the final product. The MP@FNPs of this invention, by integrating pH-responsive release, self-supply of hydrogen peroxide and oxygen, and continuous GSH depletion functions, can specifically activate a self-maintaining cascade reaction in the tumor microenvironment, disrupting the redox homeostasis of tumor cells and inducing ferroptosis, thereby effectively overcoming the resistance of tumor cells to platinum-based drugs and synergistically enhancing the efficacy of chemotherapy-immunotherapy.

The present invention relates to a conjugate for use in the treatment of cancer, the conjugate comprising a first moiety A selected from metal chelating agents, a second moiety B selected from lysosomotropic agents; and a linker L that binds moieties A and B together. The invention also relates to their use in the pharmaceutical field, in particular in a method for the treatment of cancer.

This invention discloses the application of SDC1 in the diagnosis and treatment of breast cancer. Through bioinformatics analysis, cell function experiments, multi-omics analysis, and animal model validation, this invention reveals for the first time the high expression of SDC1 in breast cancer and its correlation with poor patient prognosis. It elucidates the molecular mechanism by which SDC1 promotes the malignant progression of breast cancer by regulating ECM remodeling, EMT, angiogenesis, and ferroptosis resistance, and verifies the therapeutic potential of MZ1 in inhibiting breast cancer growth and metastasis by downregulating SDC1 expression. This invention provides the application of reagents for detecting SDC1 expression levels in the preparation of diagnostic or prognostic kits for breast cancer, as well as the application of SDC1 inhibitors in the preparation of drugs for treating breast cancer. This invention provides new technical solutions for the diagnosis, prognostic assessment, and treatment of breast cancer.

The present application relates to the technical field of nano-preparation, in particular to an extracellular vesicle-liposome hybrid nanoparticle and a preparation method and application thereof. The extracellular vesicle-liposome hybrid nanoparticle provided by the present application significantly improves the ability of drugs to cross the blood-brain barrier and the target enrichment efficiency of ischemic lesions in the brain through active targeting modification; the specific response release of drugs is realized by using the high active oxygen microenvironment of the lesion, non-specific distribution of drugs is reduced, and the systemic toxic side effects are reduced; ultimately, a multi-target point synergistic treatment system capable of synchronously regulating neural cell apoptosis, glial cell inflammatory activation, brain microvascular endothelial cell ferroptosis and the structural integrity of the blood-brain barrier is constructed, the problem that the effect of traditional single target point intervention is limited is broken through from the root, and a more efficient, safe and precise new treatment strategy is provided for cerebral ischemia-reperfusion injury.

The application discloses application of FBXO2 in colorectal cancer and prognosis judgment. Specifically, the application finds the role of FBXO2-FABP5 axis in p53-mediated colorectal cancer ferroptosis resistance: p53-activated FBXO2 promotes lysosomal degradation of FABP5 through the CMA pathway, leading to a decrease in PUFA levels, and ultimately leading to colorectal cancer ferroptosis resistance. Therefore, FBXO2 protein and FABP5 can be used as new colorectal cancer diagnostic markers.

This invention belongs to the fields of biomedicine and molecular biology, focusing on the application of NAT10 and related biomolecules in the diagnosis and treatment of deep vein thrombosis (DVT). Specifically, this invention has found that NAT10 is a key initiator of endothelial cell ferroptosis, and its expression is significantly increased in DVT. The results indicate that inhibiting NAT10 reduces ac4C levels in DVT, thereby alleviating endothelial ferroptosis. However, decreased NAT10 expression leads to reduced HMOX1 stability and decreased Fe... 2+ The release and inhibition of lipid peroxidation make targeting the NAT10 / HMOX1 axis a potential treatment for DVT, and therefore this invention has good potential practical application value.

The application discloses application of an IRS1 gene promoter region SNP site as a pig sexual maturity molecular genetic marker. The present application takes the IRS1 gene promoter region as a research object, and studies the correlation between the IRS1 gene promoter region and sow sexual maturity by using molecular and cell biology methods: it is found that g.128307611C>A and g.128307308C>T are significantly correlated with the age of sexual maturity of Duhei pig populations; then, the influence of different genotypes of the above sites on the activity of the IRS1 gene promoter is studied by transfecting different vectors. Further, the sow ovarian granulosa cells are taken as experimental materials, and experimental techniques such as transcriptome sequencing, total iron colorimetry and malondialdehyde colorimetry are used to study the influence of the IRS1 gene on the transcription level and ferroptosis of the sow ovarian granulosa cells, and it is found that the IRS1 gene influences the different genes of the cell transcriptome, and is mainly enriched in signal pathways such as iron ion homeostasis, and inhibits the ferroptosis of the cells.

This invention relates to antimony nanopowder, its preparation method, and its applications, belonging to the field of metal powder processing technology. The method includes dispersing antimony nanopowder in a solvent to obtain a dispersion, mixing the dispersion with 5-10 times the mass of nitrobenzene diazonium salt (p-NBD) of the antimony nanopowder, and reacting under light irradiation at 0-4°C for 30-60 hours to obtain passivated antimony nanopowder. The diazo chemical reaction forms stable covalent bonds on the surface of Sb NPs, blocking their interaction with respiratory cells. Compared with the original Sb NPs group, the nitrobenzene diazonium salt modification reverses the GPX4 activity inhibition effect, upregulates GPX4 protein expression and restores it to near the control group level, and eliminates the ability to induce ferroptosis, thus addressing the pulmonary toxicity problem of Sb NPs from the perspective of ferroptosis mechanism.

The application provides a multifunctional nano drug delivery system based on iron-doped MOF and a preparation method and application thereof. The system comprises: an Fe / MOF core loaded with a chemotherapeutic drug and an HO-1 inhibitor; a PDA coating layer coated on the surface of the Fe / MOF core for providing near-infrared light heat conversion capability and surface modification interface; and E3 aptamer covalently coupled on the PDA coating layer, constituting a synergistic nano platform with active targeting, pH / NIR dual-responsive drug release, chemical kinetics therapy, ferroptosis sensitization, photothermal therapy and immune regulation functions. The nano system can realize efficient accumulation at the tumor site through active targeting mediated by E3 aptamer, and controllably release drugs under an acidic microenvironment or near-infrared light. A new strategy for multi-mechanism synergistic treatment is provided to overcome the multiple drug resistance and immunosuppression of mCRPC, and has important clinical application prospects.

This invention discloses an injectable hydrogel-MOF nanozyme composite formulation (G@ZnFe-Gel), its preparation method, and its application in pancreatic cancer immunotherapy. Specifically, the system is constructed from a Zn / Fe bimetallic MOF nanozyme loaded with glucose oxidase (GOD) and a Pluronic F127 / sodium alginate thermosensitive hydrogel. It exists as an injectable sol at 4°C and rapidly gels in situ at 37°C, achieving long-term retention and controlled release of the nanozyme. This system amplifies reactive oxygen species through a GOD-Fenton-like cascade catalysis, inducing ferroptosis in pancreatic cancer cells; the mitochondrial DNA released during ferroptosis is then absorbed into the ZnFe nanozyme. 2+ This invention synergistically activates the cGAS-STING pathway, promoting immune activation and transforming immune-cold pancreatic cancer into immune-hot tumors. In vitro and in vivo experiments have demonstrated that this system significantly inhibits pancreatic cancer growth, reshapes the immune microenvironment, and exhibits high biosafety and ease of preparation. This invention provides a novel, safe, and highly effective immunotherapy strategy for pancreatic cancer, featuring in situ delivery and multi-mechanism synergy, and holds promising clinical translational potential.

The application belongs to the field of biological medicine, and discloses application of an RNA helicase DHX33 inhibitor in preparation of a drug for treating or adjuvant treating thyroid cancer. The application establishes an important role of DHX33 protein in development of thyroid cancer, and provides an inhibitor having an action of inhibiting DHX33 helicase activity, thereby causing lipid peroxidation mediated by DHX33 deletion, and inducing interleukin 24 (IL-24) expression in thyroid cancer cells. The inhibitor can rapidly induce cancer cell ferroptosis, and significantly inhibit thyroid cancer cell proliferation through up-regulation of IL-24, and therefore has important medical development value.