51 results about "SLC7A11" patented technology

The invention relates to the technical field of life science, in particular to a method for constructing an atrophic gastritis-based SPEM lesion model, which comprises the following steps: S1, constructing an Slc7a11 conditional knockout mouse strain: carrying out cage hybridization on an Slc7a11 flox / flox mouse and an ATP4b-Cre transgenic mouse, and knocking out a gastric wall cell specific Slc7a11 gene; s2, carrying out genotyping identification; the identification method based on the atrophic gastritis SPEM lesion model and the construction method based on the atrophic gastritis SPEM lesion model comprise the following steps: S1, pathological model verification: taking a mouse gastric mucosa tissue slice, quantitatively analyzing the proportion of an SPEM region by adopting an immunofluorescence double-standard technology, and confirming Slc7a11 knockout induced SPEM pathological characteristics in combination with the existence of SPEM in the gastric mucosa; and S2, long-term pathology evolution monitoring. Through gastric wall cell specific Slc7a11 gene knockout and multiple PCR identification technologies, the initial response SPEM state after gastric mucosa damage is successfully simulated, and the kit is used for researching atrophic gastritis pathological mechanisms and evaluating drug intervention.

The invention relates to a CAR-T (Chimeric Antigen Receptor-T) cell targeting SLC7A11.

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 invention discloses a combination of a glutathione synthesis inhibitor and a glucose uptake inhibitor, a nanoparticle delivery system and application thereof, and belongs to the field of medicines. The invention proves that the SLC7A11 is remarkably overexpressed in lung adenocarcinoma and is related to poor clinical prognosis; experiments find that the combination of the glutathione synthesis inhibitor and the glucose uptake inhibitor shows an effect of enhancing lung adenocarcinoma treatment in medium and high SLC7A11 expression cells, and can also achieve an effect equivalent to glucose deprivation under the condition of SLC7A11 overexpression in low expression cells. In order to optimize a delivery mode and minimize systemic toxicity, the invention also prepares a dual-cell membrane coated dual-drug nanoparticle delivery system, the system shows the ability to enhance tumor targeting and drug controllable release, effectively solves the problem of expression difference (heterogeneity) of SLC7A11 in tumors, and shows a significant anti-tumor effect in a preclinical model, and the system has good application prospects. And a promising treatment method is provided for treating lung adenocarcinoma.

The invention discloses an application of an NRF2 signal channel activator in preparation of a medicine for preventing or treating hyperuricemia-related atherosclerosis, relates to the technical field of medicines, and particularly relates to an application of the NRF2 signal channel activator in preparation of a medicine for preventing or treating hyperuricemia-related atherosclerosis. The NRF2 signal channel activator is used for up-regulating NRF2 protein expression or enhancing transcriptional activity of the NRF2 protein; the NRF2 signal channel activator is used for up-regulating expression of a downstream target gene SLC7A11 and / or GPX4 so as to inhibit ferroptosis of hyperuricemia aortic macrophages; the level of glutathione (GSH) in serum is increased; the malondialdehyde (MDA) and / or iron ion (Fe < 2 + >) level in serum is reduced; nRF2 signal channel activation and macrophage ferroptosis inhibition are associated, and the NRF2 signal channel is applied to prevention and treatment medicines for hyperuricemia-related atherosclerosis, so that development of specific treatment medicines for patients suffering from hyperuricemia-related atherosclerosis is facilitated.

The invention provides an oligopeptide, and a lentiviral expression vector and a recombinant cell for expressing the oligopeptide. The invention further provides application of the compound in tumor treatment. After the oligopeptide is delivered to HT1080 cells through a lentivirus system, the intracellular SLC7A11 protein level is reduced, the intracellular Fe < 2 + > and lipid peroxidation level is remarkably increased, and the oligopeptide has a remarkable inhibition effect on cell proliferation and has the tumor treatment potential.

The invention belongs to the field of biological medicine, and particularly relates to application of a compound in preparation of a medicine for preventing and treating aortic dissection, the compound is nobiletin, the chemical name of the compound is 3 ', 4', 5, 6, 7, 8-hexamethoxyflavone, and the CAS number is 478-01-3. The invention also correspondingly provides a pharmaceutical composition. The death rate of aortic dissection is high, treatment depends on surgical treatment, and the death rate is extremely high. At present, an effective medicine for preventing and treating the aortic dissection is lacked clinically, the nobiletin is screened and determined to be used as the medicine for preventing and treating the aortic dissection, the molecular mechanism of the nobiletin is clear that the nobiletin targets ferroptosis related protein SLC7A11 to improve ferroptosis of vascular smooth muscle cells, namely VSMC, and a new target spot is provided for treatment of the aortic dissection.

The invention relates to application of PFOI in preparation of a medicine for inducing tumor cell ferroptosis, and belongs to the technical field of medicine. The invention provides application of PFOI in preparation of a medicine for inducing tumor cell ferroptosis. The invention verifies the correlation between PFOI and tumor cell ferroptosis through experiments, and proves that PFOI can cause cancer cell mitochondrial atrophy, membrane density increase and mitochondrial ridge reduction; the ROS of cancer cells is increased; regulating cancer cell GSH metabolism and fatty acid biosynthesis, resulting in GSH depletion and lipid deposition; the ferroptosis of cancer cells is promoted by inhibiting the expression of the SLC7A11. On the basis, the invention provides a new application of PFOI in inducing tumor cell ferroptosis, an experimental basis and a new treatment strategy are provided for clinical treatment of cancers, and a new technical support is provided for targeted treatment of cancers.

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.

The invention discloses application of lentinan in preparation of a macrophage ferroptosis inhibitor, and belongs to the technical field of biological medicines. Animal experiments prove that the LNT can play a role in treating atherosclerosis by inhibiting ferroptosis of macrophages. In-vitro experiments prove that LNT has the effect of inhibiting lipid deposition and ferroptosis of macrophages caused by ox-LDL from macrophages which are keys for regulating and controlling atherosclerosis, and prove that LNT is a natural product for inhibiting ferroptosis, and Slc7a11 is further screened as a target gene for regulating and controlling ferroptosis of macrophages by LNT. A drug target and a new theory are provided for effective prevention and treatment of atherosclerosis, and a theoretical foundation is laid for developing LNT into a drug for clinical treatment of atherosclerosis.

The invention belongs to the technical field of gene drugs, and particularly relates to application of lncRNA-AU020206 in preparation of drugs for treating cerebral arterial thrombosis, the key effect of the lncRNA-AU020206 in occurrence and development of the cerebral arterial thrombosis is disclosed for the first time, and it is clear that the lncRNA-AU020206 activates ferroptosis signal channels through negative regulation of SLC7A11 expression, so that cerebral ischemia reperfusion injury is aggravated. In-vivo and in-vitro experiments prove that the levels of MDA, ROS and Fe < 2 + > can be remarkably reduced by silencing the lncRNA-AU020206, the expression of GPX4 and SLC7A11 can be up-regulated, the cerebral infarction volume and neurological dysfunction can be reduced, and cerebral edema and apoptosis can be improved. Therefore, the lncRNA-AU020206 not only can be used as a new target for treating the cerebral arterial thrombosis, but also can be used for developing a related diagnostic kit, and has remarkable clinical application prospect and market value.

An aryl heterocyclic SLC7A11 inhibitor, and a preparation method therefor and the use thereof. The new SLC7A11 inhibitor can be used for preventing and / or treating diseases related to SLC7A11, for example, tumors such as pancreatic cancer, liver cancer, osteosarcoma and glioma, chronic diseases such as fatty liver, cirrhosis, hepatic fibrosis, pulmonary fibrosis and diabetic skin damage, or neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease.

The invention discloses a preparation method of a radix tetrastigme extract and an application of the radix tetrastigme extract in a medicine for inhibiting epithelial cell ferroptosis and pyroptosis in double ways, and mainly discloses an application of the radix tetrastigme extract in a medicine for inhibiting epithelial cell ferroptosis and pyroptosis in double ways. Comprising the following components: kaempferol-3-carveosyl glucose-7-rhamnoside and kaempferol-3-glucose-7-rhamnoside. In the technical scheme, the radix tetrastigme root hair extract can inhibit an SLC7A11 / GPX4 signal channel and an NLRP3 / GSDMD signal channel at the same time by up-regulating the protein expression levels of SLC7A11 and GPX4 and down-regulating the protein expression levels of NLRP3 and GSDMD-N at the same time, so that the radix tetrastigme root hair extract has a double-channel inhibition effect on ferroptosis and pyroptosis of epithelial cells at the same time; according to the scheme, the unique kaempferol-3-apiosyl glucose-7-rhamnoside and kaempferol-3-glucose-7-rhamnoside are extracted from the radix tetrastigme root hair, the extraction process is optimized, and the radix tetrastigme root hair with high purity is obtained through separation and effectively utilized.

The invention belongs to the field of biological medicine, and discloses application of Galectin13 recombinant protein and mimic peptide thereof in preparation of antitumor drugs. The inventor finds that the Gal13 recombinant protein and the mimic peptide HYNEYEIKVNGIRIYGFV of the Gal13 recombinant protein can be combined with CD44, so that the combination of the CD44 and SLC7A11 is blocked, and the ferroptosis sensitivity of tumor cells is enhanced. The Gal13 recombinant protein and the mimic peptide thereof are combined with Erastin to strongly induce ferroptosis. Animal experiment data show that the Gal13 recombinant protein and the mimic peptide thereof significantly promote tumor cell ferroptosis mediated by radiotherapy or immunotherapy, and greatly enhance the curative effect of radiotherapy or immunotherapy. The Gal13 recombinant protein and the mimic peptide thereof have good patent medicine prospects, and can be clinically combined with radiotherapy or immunotherapy in the future.

The invention provides a core-shell fiber. The core-shell fiber comprises a core and a shell layer which are coaxial, the core is formed by loading an SLC7A11 inhibitor on a hydrophobic polymer; a shell layer is formed by loading nano-enzyme on a hydrophilic polymer; the weight ratio of the nano enzyme to the SLC7A11 inhibitor is not less than 200; the SLC7A11 inhibitor is any one or a mixture of more than two of HG106, sulfasalazine or ilastine imidazolate, and the nano-enzyme is any one or a mixture of more than two of iridium nano-enzyme (Ir NPs), Mn3O4 nano-enzyme or Cu-TCPP (Fe) nano-enzyme. The invention also provides a dressing composed of the core-shell fiber. The invention also provides a method for preparing the core-shell fiber and application of the core-shell fiber in preparation of a wound or wound surface treatment material. The core-shell fiber and the dressing disclosed by the invention can enhance the effect of an inhibitor on a wound surface with high expression of SLC7A11, have the functions of reducing toxicity and enhancing efficacy, and can promote the healing of the wound surface.

The invention discloses a fetal growth restriction diagnostic reagent and method based on METTL1 regulation and control of SLC7A11 m7G modification. The diagnostic reagent comprises a reagent for specifically detecting the expression level of an METTL1 gene and a reagent for detecting the m7G modification level of the SLC7A11 gene. The diagnosis method comprises the following steps: collecting a placenta tissue sample of a pregnant woman, respectively detecting the m7G modification level of an SLC7A11 gene and the expression level of an METTL1 gene by utilizing a MeRIP-seq technology and a real-time fluorescent quantitative PCR technology, and realizing the diagnosis on the fetal growth limitation by combining the detection results of the m7G modification level and the expression level. By researching the m7G modification regulation mechanism of METTL1 to SLC7A11, a novel diagnostic marker and a novel diagnostic method are provided for fetal growth limitation, and the marker has the advantages of high specificity, high sensitivity, accurate result and the like, and can be widely applied to early diagnosis of clinical fetal growth limitation.

The present invention provides a polypeptide circCCDC7 241aa For use in the treatment of prostate cancer, the polypeptide comprises the amino acid sequence shown in SEQ ID NO. 2; or a sequence comprising the amino acid sequence shown in SEQ ID NO. 2 with one or more amino acids substituted, deleted, or added, and having the same function. The present invention discovered that the polypeptide acts on the SLC7A11 protein of tumor cells, inducing ferroptosis in prostate cancer cells by ubiquitination and degradation of the SLC7A11 protein, thereby effectively inhibiting the growth and progression of prostate cancer without significantly damaging normal tissues. While maintaining excellent anti-tumor properties, it also makes up for the shortcomings of traditional chemotherapy drugs with many side effects, and has good prospects for clinical translation.

The invention belongs to the technical field of medicine, and particularly relates to application of emodin in medicine for treating acute kidney injury, the medicine for treating acute kidney injury is a preparation for inhibiting kidney iron sagging, and inhibition of kidney iron sagging specifically refers to activation of SIRT3, reduction of PINK1 acetylation level, up-regulation of glutathione peroxidase GPX4 and SLC7A11 expression level and reduction of transferrin TF expression level. The ROS level of lipid active oxygen is inhibited, so that the effect of treating the acute kidney injury caused by iron poisoning is achieved.

The invention discloses an application of MSTN (myostatin) and a downstream target gene thereof as a target spot for detecting and treating liver aging, and belongs to the technical field of biological medicines. The downstream target gene disclosed by the invention is an Slc7a11 gene. The research finds that in mouse primary hepatocytes treated by MSTN recombinant protein for 24 hours, the expression of senescence markers p53, p21, p16 and gamma-H2AX is remarkably up-regulated, and the activity of beta-galactosidase is synchronously enhanced. RNA sequencing analysis shows that cell senescence related gene sets in an MSTN treatment group are remarkably enriched in GO function annotation and GSEA analysis. Differential expression gene heat map analysis further reveals that Slc7a11 is the most significant target gene for down-regulation. Therefore, the MSTN and the downstream target gene Slc7a11 thereof can be used for preparing a reagent and a kit for detecting liver aging; the composition is used for preparing medicines for treating liver aging.

The invention discloses a research method for improving depression by influence of movement on hippocampus, and relates to the field of medical science. Comprising the following steps: grouping experimental animals and constructing a model, selecting animal groups, and establishing a CUMS depression model; performing swimming exercise intervention, setting training parameters, and performing intervention by using an inhibitor; sample collection and molecular detection: anesthetizing animals, taking hippocampus tissues, and carrying out ferroptosis index detection, protein and gene expression analysis and neuron morphology observation on the hippocampus tissues; data analysis and mechanism verification are carried out, and behavioristics and molecular index correlation analysis and path blocking experiments are carried out respectively. According to the invention, the ferroptosis mechanism is associated with the motion anti-depression effect for the first time, the hub effect of the Nrf2 / SLC7A11 / GPX4 pathway is disclosed, behavioristics, molecular biology and ultrastructure analysis are integrated, a multi-dimensional verification system is established, quantifiable motion intervention parameters are provided, and a basis is provided for formulating a clinical motion prescription.

The invention belongs to the field of biological pharmacy, and particularly relates to application of maslinic acid as a cis-platinum toxicity protective agent. The maslinic acid disclosed by the invention can be used for preventing ototoxicity induced by cis-platinum by recovering the activity of mouse cochlear hair cells SLC7A11, and can be used for repairing mouse hearing impairment induced by cis-platinum. Experimental results show that maslinic acid can recover activity reduction of SLC7A11 caused by cis-platinum, so that the level of LPO in cells is reduced, the survival rate of HEI-OC1 cells is increased, and the anti-cancer effect of cis-platinum is not affected; animal experiments also show that maslinic acid can inhibit mouse hearing impairment induced by cis-platinum. Therefore, maslinic acid can reduce the ear toxicity of cis-platinum and exert an inner ear protection effect.

The invention relates to a humanized antibody targeting SLC7A11 and a CAR-T cell constructed by the humanized antibody.

The application relates to application of PFOI in preparation of a tumor cell ferroptosis-inducing drug and belongs to the technical field of medicines. The application provides application of PFOI in preparation of a tumor cell ferroptosis-inducing drug. The application verifies the correlation between PFOI and tumor cell ferroptosis through experiments, proves that PFOI can cause mitochondrial atrophy, membrane density increase and mitochondrial cristae reduction of cancer cells, cause ROS increase of the cancer cells, regulate GSH metabolism and fatty acid biosynthesis of the cancer cells, cause GSH exhaustion and lipid deposition, and promote the cancer cells to occur ferroptosis by inhibiting the expression of SLC7A11. Based on this, the application provides a new use of PFOI for inducing tumor cell ferroptosis, provides experimental basis and a new treatment strategy for clinical treatment of cancer, and provides new technical support for targeted treatment of cancer.

The use of the expression levels of at least three biomarkers selected from the group of SLC7A11, SERPINE1, PSAT1, PHGDH-1, TXNRD1, VIM, SNAI1, ZEB1, NANOG, SOX2, PCK2, G6PD, ASNS, NUPR1 and SLC6A9 as a molecular signature for identifying an individual with cancer, in particular breast cancer, as being susceptible to respond to a treatment by a mitochondria-targeted antioxidant.

The invention relates to an aryl heterocyclic SLC7A11 inhibitor and a preparation method and application thereof, and the novel SLC7A11 inhibitor can be used for preventing and / or treating diseases related to SLC7A11, such as pancreatic cancer, liver cancer, osteosarcoma, glioma and other tumors and chronic diseases such as fatty liver, liver cirrhosis, hepatic fibrosis, pulmonary fibrosis, diabetic skin injury and the like. Or amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease and other neurodegenerative diseases.

The invention discloses a antler active peptide fragment as well as a preparation method and application thereof, and relates to the technical field of biological peptides. The amino acid sequence of the antler active peptide fragment is NGYDFGFDGDFYAR, and the antler active peptide fragment not only has the effect of promoting proliferation of osteoblasts, but also can inhibit reduction of cell viability and relieve osteoblast damage. Meanwhile, the antler active peptide fragment can effectively antagonize DEX-induced ferroptosis and recover the physiological function of osteoblasts to a certain extent. Specifically, the antler active peptide fragment can reduce the ROS level of osteoblasts, reduce the MDA and LPO content and iron ion accumulation, and promote the expression of osteogenic proteins Runx2 and Osterix in osteoblasts and the callback of ferroptosis proteins SLC7A11 and GPX4.

This invention discloses a novel application of undecanoic acid in inducing ferroptosis in laryngeal cancer cells and in the preparation of anti-laryngeal cancer drugs. For the first time, it was discovered that the known compound undecanoic acid can specifically target the mitochondria of laryngeal cancer cells, inducing mitochondrial structural damage and dysfunction. This, in turn, activates the ferroptosis pathway through multiple mechanisms, including increasing intracellular ferrous ion accumulation, increasing lipid peroxide levels, downregulating GPX4 / SLC7A11 expression, and upregulating ACSL4 expression, thereby effectively inhibiting the proliferation of laryngeal cancer cells. Based on this mechanism, this invention provides a pharmaceutical composition with undecanoic acid as the active ingredient, and its combined application with platinum-based drugs (such as cisplatin). This combined treatment exhibits a significant synergistic effect, particularly overcoming the platinum resistance of laryngeal cancer cells. This invention provides a novel drug selection and combination therapy strategy for the treatment and prevention of laryngeal cancer and precancerous lesions.

The application belongs to the field of biological pharmacy, and particularly relates to application of maslinic acid as a cisplatin ototoxicity protective agent. The application discloses that maslinic acid can prevent cisplatin-induced ototoxicity by restoring the activity of mouse cochlea hair cells SLC7A11, and can repair cisplatin-induced hearing impairment in mice. Experimental results show that maslinic acid can restore the reduced activity of SLC7A11 caused by cisplatin, thereby reducing the intracellular LPO level, increasing the HEI-OC1 cell survival rate, and not affecting the anticancer effect of cisplatin; animal experiments also show that maslinic acid can inhibit cisplatin-induced hearing impairment in mice. Therefore, maslinic acid can reduce the ototoxicity of cisplatin and play an inner ear protection role.

A method for predicting disease free status or overall survival in an individual diagnosed with cancer, the method comprising a step of assaying a biological sample from the individual for expression levels of at least one gene, or a protein encoded by said gene, selected from ATP5B, GPX4, SLC7A11, IREB2, SLC3A2, GCLM, ACSL3, NQO1, AIFM2, HMOX1, POR, CysLT1, CysLT2 and CTH; wherein when the expression levels of at least one gene, or a protein encoded by said gene, selected from ATP5B, GPX4, SLC7A11, IREB2, SLC3A2, GCLM, ACSL3, NQO1, AIFM2, HMOX1, POR, CysLT1, CysLT2, and CTH is dysregulated relative to a reference value for at least one gene, or a protein encoded by said gene, selected from ATP5B, GPX4, SLC7A11, IREB2, SLC3A2, GCLM, ACSL3, NQO1, AIFM2, HMOX1, POR, CysLT1, CysLT2, and CTH assayed from a biological sample from the subject with no cancer, the individual is predicted to have an increased probability of having disease free status and having an increased chance of overall survival.