90 results about "Cellular senescence" patented technology

The invention provides a construction method of a predictive cell senescence model, a method for predicting the senescence state of a tissue sample based on the senescence model, a method for screening potential therapeutic drugs, equipment, a medium and a program product, and relates to the field of intelligent medical treatment. The model construction method comprises the following steps: acquiring a training set sample expression profile data set; identifying a key senescence gene set from the data set by using a feature selection algorithm; inputting the key senescence gene set into a machine learning model to fit a prediction model, and determining an optimal hyper-parameter to obtain a cell senescence model containing the weight of a single gene in the key senescence gene set; the cell senescence model is a senescence score obtained by calculating the sum of the product of the expression quantity of a single gene and the regression coefficient thereof. The cell senescence model, namely PreCSenM, is constructed by integrating a plurality of senescence characteristic gene sets and a gene scoring algorithm, the accuracy in CS evaluation is superior to that of 10 existing methods, and the application of CS from biological research to clinical scenes is also realized.

The present invention relates to a compound for inducing the expression of the anti-aging gene klotho and a preparation method therefor. The compound represented by Chemical Formula 1, according to the present invention, has an excellent effect of increasing the expression level of the klotho gene which is a gene associated with aging, and thus can be useful for a pharmaceutical composition, cosmetic composition or food composition for preventing skin aging, inhibiting cellular senescence or preventing, treating alleviating a vascular aging-induced disease or a renal disease.

The invention discloses a combined pharmaceutical composition for preventing, relieving or treating acute myelogenous leukemia and application, and relates to the technical field of biomedicine. The invention provides a combined pharmaceutical composition for preventing, relieving or treating acute myelogenous leukemia. The combined pharmaceutical composition comprises vincristine and cytarabine or pharmaceutically acceptable salts and solvates of the vincristine and the cytarabine. According to the vincristine and cytarabine combined pharmaceutical composition, the apoptosis level of acute myelogenous leukemia cells can be remarkably improved, and compared with single-drug treatment, the vincristine and cytarabine combined pharmaceutical composition has higher anti-tumor efficacy; vincristine interferes or blocks a cell senescence state induced by cytarabine through a microtubule destruction effect, so that the problem of drug insensitivity caused by cell senescence is solved, and drug resistance caused by cell senescence is effectively reversed.

This invention relates to the field of biotechnology, specifically disclosing an aging biomarker capable of marking cellular senescence and its applications. The purpose of this invention is to provide a novel biomarker for assessing cellular senescence and its applications, aiming to address the problem of the lack of highly specific biomarkers for the senescence status of immune cells in tumor tissues in existing technologies, particularly the technical bottleneck of accurately assessing the degree of immune cell senescence in the complex tumor microenvironment.

The present invention describes for the first time a method for preventing and / or reversing the phenomenon of premature senescence of skin cells and complex chronic wounds, characterized in that an effective amount of the growth hormone secretagogue peptide GHRP6 is applied. Also object of the present invention is a method for treating cases of complex chronic wounds that have developed primary or secondary refractoriness caused by the development of a cellular senescence process, transforming them from refractory wounds to responsive wounds in the presence of proliferative agents with which they unexpectedly manage to reverse and restart the healing process. Complex chronic wounds include cases of diabetic foot ulcers, venous ulcers, pressure ulcers, radiation ulcers, and other types of chronic wounds that are characterized by refractoriness to all types of treatment. These cases currently have no effective treatments.

The invention discloses a lactobacillus paragasseri strain capable of converting anthocyanin to generate various active metabolites, inhibiting NF-kappa B and cGAS-STING signals and enhancing inflammatory response relieving, and belongs to the technical field of microorganisms and the technical field of medicines. The lactobacillus paragasseri CCFM1499 provided by the invention can be used for converting anthocyanin into various active substances such as homovanillic acid, cyanidin, 3 ', 4'-dihydroxyphenylacetic acid and the like; fermentation supernate obtained by fermenting anthocyanin through the lactobacillus paragasseri CCFM1499 has the following effects: (1) the capability of reducing inflammatory factors of cells is achieved; (2) the cell senescence phenotypic capability is relieved; (3) the cGAS-STING signal channel capability is inhibited; and (4) inhibiting the NF-kappa B signal path capability. The lactobacillus paragasseri CCFM1499 fermented anthocyanin provided by the invention can be used for preparing a product for relieving inflammatory response, and has a huge application prospect.

The MYC and NMYC transcription factors (TFs) play a key role in cell proliferation and are overexpressed in most cancer cells. However, in normal cells their overexpression triggers safeguard mechanisms promoting cell death and cellular senescence, which are bypassed in cancer cells. Here, the inventors reveal that in normal cells MYC binds to the Inositol 1,4,5-Trisphosphate Receptor type 1 (ITPR1) gene and upregulates its expression, triggering an ER-mitochondria calcium (Ca2+) transfer, which is involved in MYC-induced cell death and senescence. Supporting a tumor suppressive role of MYC / ITPR1 axis, ITPR1 expression is generally decreased in cancer and reactivation of this pathway induces cancer cell death. Nevertheless, some cancer cells, generally expressing high levels of MYCN and / or MYC, also express high level of ITPR1, which correlates with high expression of BCL2, encoding an inhibitor of ITPR1. Strikingly, in high-risk MYCN-amplified neuroblastoma, ITPR1 expression is controlled by NMYC and its level correlates with worse patient survival. In these cells, blocking the interaction between BCL2 and ITPR1, via an BCL2-BH4 domain inhibitor induces mitochondrial Ca2+ accumulation and cell death, and decreases tumor size. Thus, the present invention relates to a method for treating MYChigh cancer, and in particular NMYC--amplified neuroblastoma in a subject by administering an BCL2-BH4 domain inhibitor.

The invention discloses an application of miR-26a-5p in preparation of a product for preventing, repairing or treating cell aging. According to the invention, miR-26a-5p is applied to preparation of products for preventing and treating cell aging for the first time, a brand new molecular intervention strategy is provided for cell aging resistance, and the problem of lack of targeted molecular targeting schemes in the prior art is effectively overcome. The miR-26a-5p can be used for remarkably regulating and controlling the expression of cell cycle key factors CDK1, p21, Ki67 and Lamin B1, so that the proliferation state and the aging process of cells are accurately intervened.

This invention discloses the application of lipoic acid analog formulations in the preparation of anti-cardiomyocyte senescence products. The lipoic acid analog DMAE-LA is N-(2-(dimethylamino)ethyl)-5-(1,2-dithiopentane-3-yl)pentanamide, with a concentration of 2-25 μM. DMAE-LA pretreatment effectively reduces intracellular ROS, improves mitochondrial function, inhibits the overexpression of p21 and HMGB1, and restores Lamin B1 levels, thereby alleviating the senescent manifestations of cardiomyocytes. DMAE-LA reduces H₂S oxidative depletion by inhibiting ROS generation and may promote H₂S synthase activity, increasing endogenous H₂S levels and further enhancing cellular antioxidant capacity. In summary, DMAE-LA can significantly inhibit cardiomyocyte senescence through multiple antioxidant mechanisms and organelle function protection, providing a potential intervention strategy for targeting cellular senescence in cardiovascular diseases.

The invention discloses an NK cell culture solution and culture and application of NK cells, the NK cell culture solution comprises an activation culture solution and an amplification culture solution, the activation culture solution and the amplification culture solution respectively contain a basal culture medium and respective corresponding cell factors, and the activation culture solution also contains calycosin with the final concentration of 0.1-10 [mu] g / mL and formononetin with the final concentration of 1-20 [mu] g / mL; the amplification culture solution also contains astragaloside IV and soyasaponin I. The components such as calycosin, formononetin, astragaloside IV and soyasaponin I added into the NK cell culture fluid can maintain stable and lasting physiological activity of NK cells and slow down cell senescence, so that secretion of cell factors is promoted, the secretion level of the cell factors is higher, and the purposes of enhancing the persistence of cell activity and improving the killing rate of the NK cells are achieved.

The invention provides a composition for delaying cell senescence as well as a preparation method and application thereof, and belongs to the technical field of medicines. The preparation method comprises the following steps: loading tea polyphenol on a dog bone marrow mesenchymal stem cell exosome, and modifying the surface of the dog bone marrow mesenchymal stem cell exosome with arginine nonamer to prepare a modified tea polyphenol-loaded exosome; the preparation method comprises the following steps of: modifying cholesterol by using arginine nonamer, and preparing lipidosome by using the cholesterol modified by the arginine nonamer, DSPE-PEG2000, phospholipid embedded resveratrol and epigallotein gallate; polysaccharide is extracted from rhizoma polygonati, fructus lycii and ginseng, and rhizoma polygonati / fructus lycii / ginseng polysaccharide is prepared; the preparation method comprises the following steps: mixing an acellular dermal matrix with polygonatum sibiricum / medlar / ginseng polysaccharide, adding lipidosome and a modified tea polyphenol-loaded exosome, co-incubating, and freeze-drying to prepare the composition for delaying cell aging, the composition has a better drug embedding effect, can improve the stability and transdermal absorption effect of the drug, has better antioxidant, antibacterial and anti-inflammatory effects, and can be used for preparing the medicine for delaying cell aging. The effect of delaying skin cell senescence can be better achieved through multiple ways, and safety and degradability are achieved.

The invention discloses application of deaminotyrosine in improvement or prevention and treatment of muscular atrophy, and relates to the technical field of biological medicines. The invention finds that in the cellular level, DAT can effectively resist C2C12 myoblast senescence induced by etoposide; in a dexamethasone-induced C2C12 myotube atrophy model, DAT not only inhibits myotube diameter reduction from the form, but also down-regulates mRNA expression of key atrophy genes Atrogin-1 and MuRF-1 from the molecular level, and inhibits excessive activation of a ubiquitin-proteasome system; in-vivo animal experiments prove that DAT can reverse aging-related dyskinesia of rapidly-aged SAMP8 mice, and gait parameters of the rapidly-aged SAMP8 mice are all remarkably improved. According to the invention, a complete evidence chain from cells to the whole is constructed, and the DAT is proved to improve the senescent skeletal muscle atrophy through multiple ways of intervening cell senescence, antagonizing protein degradation, improving muscle microenvironment and the like, and shows important potential application value.

The invention provides high-activity polygonatum polysaccharide as well as a preparation method and application thereof, and belongs to the technical field of effective component extraction. A mixture of cellulase, hemicellulase and pectinase is used as a compound enzyme preparation for enzymolysis, extraction and purification to obtain the polygonatum polysaccharide PCPA. The molecular weight of the polygahatous polysaccharide PCPA is 1372 Da, the polygahatous polysaccharide PCPA is composed of three monosaccharides of arabinose, glucose and fructose, the molar ratio of the three monosaccharides is 0.39: 6.48: 93.13, and the polygahatous polysaccharide PCPA has the effects of delaying cell senescence and improving cell repair activity.

Disclosed are use of a circRNA molecule as a diagnostic marker in a cell senescence diagnosis kit, and use thereof as a treatment target for cell senescence. The present invention finds that circHERC1 is lowly expressed in both cell models of natural senescence and induced senescence. Overexpression of circHERC1 in endothelial cells can improve the proliferation capacity of the endothelial cells, effectively extend the telomere length of the cells, activate telomerase, reduce the β-galactosidase positive rate of the cells, and reduce the expression of all senescence-associated proteins. Introduction of exogenous circHERC1 into mice can effectively delay the senescence of various organs and the shortening of telomeres in aged mice and reduce the β-galactosidase positive rates of various organs of aged mice.

The invention belongs to the technical field of biomedicine, and relates to application of Mars2 in tissue repair and regeneration, the expression level of the Mars2 is up-regulated by more than two times through mRNA delivered by AAV9, cell senescence is delayed, cell metabolism is remodeled, and tissue rejuvenation is promoted; in-vivo and in-vitro experiments prove that the metabolism function of mitochondria can be improved, oxidative stress can be reduced and cell senescence can be delayed by up-regulating the expression of the Lars2, so that the tissue repair and regeneration capacity of the Lars2 can be enhanced; the application potential in fibroblast biology and regenerative medicine is expanded; an anti-aging strategy taking metabolic remodeling as a target spot is provided, and is different from a traditional way depending on oxidation resistance or signal path intervention; experiments prove that the regulation and control of the Mars2 have universality and are suitable for various fibroblast types and tissue environments.

The invention belongs to the technical field of tissue engineering and aging resistance, and particularly relates to a composition for delaying cell aging and maintaining tissue homeostasis as well as a preparation method and application of the composition. Specifically, research finds that adipose tissues, skin tissues and the like are placed in a serum-free basal culture medium, adherent culture is performed, the obtained supernate is collected, and the obtained serum-free conditioned culture medium preparation can effectively inhibit aging of cells (such as ADSCs or HDFs) and maintain the functional steady state of the cells in in-vitro culture. Meanwhile, the culture medium product provided by the invention is also proved to be capable of inhibiting an IL-6 / STAT3 signal channel, and the channel is revealed to be a core mechanism of the anti-aging effect of the culture medium product, so that mechanism support is provided for the application of the culture medium product to cell aging resistance, and the culture medium product has good practical application value.

The present invention relates to a composition comprising HAPLN1 as an active ingredient for preventing or treating senile degenerative brain diseases. Specifically, recombinant human HAPLN1 protein (rhHAPLN1) lowers the protein level of p16 in cultured human astrocytes to inhibit cellular senescence caused by the accumulation of beta amyloid peptides, and further inhibits phosphorylation (p-p38 MAPK) of p38 MAPK protein, thereby also having the possibility of inhibiting inflammatory responses associated with the onset of Alzheimer's disease and Parkinson's disease. In addition, the recombinant human HAPLN1 protein (rhHAPLN1) exhibits significant memory and learning improvement effects in in vivo experiments performed using a mouse acute Alzheimer's disease model, and thus can be expected to exhibit preventive and therapeutic effects against Alzheimer's disease that may occur with aging and the like. In addition, the inhibitory effect of the rhHAPLN1 protein on cellular senescence and inflammatory responses of astrocytes can provide a very important clue for establishing prevention and treatment strategies not only for aging itself but also for brain functions, motor behaviors, memory, seizures, dementia, brain tumors, and the like.

This invention relates to the field of biotechnology, specifically to compositions and their application in the preparation of drugs for the prevention and treatment of lymphoma. The invention provides a composition comprising clostridium tumefaciensin and epipitorone, which synergistically enhance the effects of targeting the LCP2-mediated IQGAP2 / LaminA / C / SUV39H1 axis to combat chemotherapy resistance in NK / T cell lymphoma. The combined use of these two drugs can significantly reverse chemotherapy resistance, providing a new treatment strategy and drug combination for relapsed / refractory NKTCL. Experimental comparisons of the efficacy of immunotherapy drugs such as PD-1 inhibitors revealed that the anti-cellular senescence drug combination of clostridium tumefaciensin and epipitorone provided by this invention is significantly more effective than PD-1 inhibitors.

The application belongs to the technical field of biological medicine, and particularly relates to application of SFRP1 in treatment of aortic aging drugs. SFRP1 can induce generation of vascular organoids, significantly antagonize vascular smooth muscle cell senescence induced by angiotensin II and bleomycin, enhance vascular smooth muscle cell activity, improve cell oxidative stress ability, reduce cell beta-galactosidase activity, reduce intracellular calcium deposition level, reduce phenotype conversion and reduce extracellular matrix remodeling. Taxifolin can significantly improve accelerated aortic aging in VSMC-specific Sfrp1 knockout mice. SFRP1 and / or Taxifolin both play an anti-aortic aging role, prevent and / or treat aortic aging related diseases. SFRP1 can be used as a screening target to screen drugs against cell senescence damage.

The invention relates to the technical field of biomedicine, and discloses a space transcriptome-based senescence sensitive site identification method, system and device and a medium, and the method comprises the following steps: obtaining senescence differential gene data of different types of sites in an organ tissue of a to-be-identified target according to a space transcriptome sequencing data set of the organ tissue of the to-be-identified target; intersecting the aging differential gene data of different types of sites in the organ tissue of the target to be identified with a preset aging gene data set to obtain aging sensitive gene data of the organ tissue of the target to be identified; obtaining an aging score of each site in the organ tissue of the to-be-identified target by using a preset identification rule, obtaining SSS in the organ tissue of the to-be-identified target by using a preset identification rule, and analyzing to obtain a microenvironment of each SSS. According to the method, the SSS and the microenvironment thereof can be identified and analyzed at high precision, and cell senescence analysis and potential intervention target determination are facilitated.

The present invention relates to compositions comprising marine derived phospholipids for ameliorating at least one aging hallmark selected from the group consisting of genomic instability, telomere shortening, an epigenetic alteration, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and deregulated nutrient sensing and intercellular communication.

This invention belongs to the field of cell engineering technology, specifically relating to an engineered mitochondrial nanoshield, its preparation method, and its applications. The engineered mitochondrial nanoshield can resist damage from high concentrations of calcium ions in the extracellular environment, and also possesses BMMSCs targeting ability and ROS-responsive characteristics. After intravenous injection, the engineered mitochondrial nanoshield can selectively target BMMSCs to alleviate cellular senescence and increase bone mass in aged mice.

The present application relates to the technical field of edge detection algorithm, and particularly relates to an end-to-end cell aging state prediction method based on nuclear membrane morphology, which comprises the following steps: step one, collecting a fluorescence image of human fibroblasts subjected to immunofluorescence staining through a fluorescence microscope; step two, performing data enhancement processing on nuclear membrane data, amplifying training data, and improving model generalization capability; step three, generating a prediction of nuclear membrane segmentation mask through a deep neural network, and obtaining mask information; and step four, simultaneously inputting the mask information into an ellipticity module, a smoothness module and a concave degree module for multi-angle calculation and evaluation. The present application evaluates nuclear membrane morphology changes from multiple angles to meet the growing demand for quantification of cell aging state in the field.

The object of the present invention is to provide a method for analyzing the disorder of collagen in living organisms. [Solution] The above problem can be solved by a screening method for cellular senescence-related substances, which includes the step of contacting a candidate substance with cells expressing procollagen C-proteinase, procollagen C-proteinase enhancer, procollagen C-proteinase-cleaved protein, procollagen N-proteinase, procollagen N-proteinase activator, or procollagen N-proteinase-cleaved protein of the present invention.

The application discloses oleanane triterpene saponin compounds with improved mitochondrial energy anti-aging, a preparation method and application thereof, and belongs to the technical field of medicines and cosmetics. Through systematic chemical component research on Zhejiang Hongshan tea flowers, two new oleanane triterpene saponin compounds CK and CL are separated, and the chemical structures are determined by using high-resolution mass spectrometry and nuclear magnetic technology. In-vitro anti-photoaging activity research shows that the new compounds CK and CL provided in the application have good protection effects on ultraviolet-induced fibroblast photoaging, can significantly improve the content of type I collagen, reduce the expression of matrix metalloproteinases mmp1 and mmp3 , increase the generation of mitochondrial autophagosomes and lysosomes, promote mitochondrial autophagy, relieve mitochondrial damage and improve cell senescence. The preparation method provided in the application is simple, and the activity is significant, so that the application is expected to be developed into a new anti-skin aging medicine or cosmetic.

Methods and apparatuses for treating a senescence related disease, disorder, or pathological condition. These methods may include identifying a cellular senescence status in a senescence related disease, disorder, or pathological condition in a subject; and treating the subject for the senescence-related disease, disorder, or conditional by vagal nerve stimulation.

The present invention relates to a composition comprising a combination of at least two cosmetic active agents, said combination of active agents preventing or reducing the loss of proteostasis, preventing or reducing micro-inflammatory processes, preventing cellular senescence, and preventing or reducing mitochondrial dysfunction and / or stimulating mitochondrial energy metabolism in skin cells The invention also relates to the cosmetic use of such a composition for increasing the longevity of skin cells and skin tissues, for preventing or reducing the loss of proteostasis, preventing or reducing micro-inflammatory processes, preventing cellular senescence and preventing or reducing mitochondrial dysfunction and / or stimulating mitochondrial energy metabolism, in skin cells. Finally, the invention relates to a nontherapeutic cosmetic process for caring for keratin materials comprising the topical application of such a composition.

The invention belongs to the technical field of biological medicines, and discloses application of beta-elemonic acid or a derivative or pharmaceutically acceptable salt thereof in preparation of medicines for regulating cell senescence and preventing and / or treating senescence-related diseases, including application as a cell senescence regulator (especially a senescence cell scavenger), and application of beta-elemonic acid or a derivative or pharmaceutically acceptable salt thereof in preparation of medicines for regulating cell senescence and preventing and / or treating senescence-related diseases. The invention also relates to application of the compound in preparation of medicines for preventing and / or treating diseases (such as organ fibrosis diseases and metabolic diseases) driven by cell aging pathology. In-vivo and in-vitro experiments prove that beta-EA can significantly reduce the number of SA-beta-gal positive senescence cells and down-regulate the expression of a core senescence marker protein p21 no matter in an in-vitro cell model or in an in-vivo pathological tissue. The invention also proves that beta-EA can reverse the degree of cell fibrosis, inhibits the transcriptional activity of an epithelial-mesenchymal transition pathway, has remarkable anti-fibrosis activity, and can be applied to treatment of organ fibrosis and other senescence-driven diseases.

The invention relates to application of a reagent for detecting the expression level of a PSIP1 gene or an encoded protein LEDGF / p75 of the PSIP1 gene to preparation of a product for evaluating the activity of systemic lupus erythematosus disease. The problem that an existing evaluation index is insufficient in sensitivity and specificity is solved. The invention also discloses a key effect of the PSIP1 gene in the pathogenesis of systemic lupus erythematosus, the relationship between reduction of the PSIP1 gene in T cells and cell cycle arrest, cell senescence and immune function abnormality is defined, and a theoretical basis is provided for targeted regulation and control of the PSIP1 to improve the functions of the T cells and delay or block disease progression; according to the invention, it is proposed for the first time that detection of the expression level of PSIP1 / LEDGF / p75 is used for evaluating the disease activity of systemic lupus erythematosus, assisting in diagnosis, predicting prognosis and monitoring the treatment effect, and a brand new tool and direction are provided for precise diagnosis, activity evaluation, prognosis judgment and future targeted treatment development of systemic lupus erythematosus.

The invention provides application of overexpressed IGF1R in preparation of a medicine for treating kidney IRI related symptoms, and relates to the technical field of biological medicine. The overexpressed IGF1R can inhibit the symptom of the cell premature senility induced by IRI in the transplantation process, a carrier of the overexpressed IGF1R is designed on the basis of the overexpressed IGF1R, and an IGF1R related agonist such as diflurosil or L-leucine can effectively inhibit the cell premature senility induced by the IRI; a new target spot and a new strategy are provided for clinically diagnosing and treating cell senescence caused by kidney IRI due to organ transplantation.