23 results about "Cellular senescence" patented technology

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.

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.

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.

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.

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 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.

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.

This invention provides a method for constructing and applying an animal model of sarcopenia, belonging to the field of animal model construction technology. This invention uses... adora2b Targeting genes, by knocking out the aforementioned adora2b Genetic constructing of a sarcopenia animal model. This invention uses CRISPANT technology to construct a knockout gene. adora2b Zebrafish model of genes adora2b Mutant zebrafish exhibit muscle atrophy and dysfunction, showing reduced muscle fluorescence area and average intensity, increased cellular senescence, and significantly decreased expression of muscle function-related genes, indicating that the mutant zebrafish have experienced muscle degeneration and dysfunction. The present invention provides… adora2b Mutant zebrafish serve as an animal model of sarcopenia. adora2b Research on the relationship between gene mutations and the pathogenesis of sarcopenia, as well as the screening of drugs for the prevention and treatment of sarcopenia, have laid a theoretical foundation.

The invention relates to application of a combination of decitabine and an anti-HER2 antibody in preparation of a medicine for treating tumors. The invention provides application of decitabine or an analogue thereof in preparation of a medicine for treating tumors in combination with an anti-HER2 (Human Epidermal Growth Factor Receptor 2) antibody. The invention also provides application of decitabine or an analogue thereof, an anti-HER2 antibody and one, more or all of a cell aging induction medicine, a ZBP1 agonist and an SETDB1 inhibitor in preparation of medicines for treating tumors. The present invention also provides pharmaceutical compositions and kits comprising decitabine or an analog thereof and an anti-HER2 antibody.

This invention discloses a method for predicting and validating the comprehensive skin toxicity of daily-use preservatives based on multi-pathway responses in keratinocyte-fibroblast co-culture, belonging to the technical field of daily chemical safety evaluation. This invention uses human keratinocytes (HaCaT) and human dermal fibroblasts (HSF) as dual targets, and assesses the mechanistic skin toxicity of preservatives through multiple endpoints including inflammation, barrier damage, cell senescence, and organelle damage, classifying them and guiding their formulation application. The method of this invention boasts high prediction accuracy, high sensitivity, high efficiency, and compliance with regulations. It overcomes the limitations of traditional methods that only focus on "cell viability," providing a panoramic analysis of the toxic action pathways of preservatives from three dimensions: gene expression (early signal), organelle damage (intermediate process), and population apoptosis (final outcome), avoiding false negatives caused by single endpoints and possessing broad application prospects.

This application discloses a system for predicting the prognosis of patients with primary liver cancer based on the molecular characteristics of senescent T cells. The system is based on the expression levels of senescence-related genes CDCA8, MCM4, and TTK in T cells removed from the patient's liver cancer tissue. The system includes a data collection module, a prognostic risk assessment module, and a prognostic judgment module. This application also discloses a method for predicting the prognosis of patients with primary liver cancer based on the above system. The prediction system and method disclosed in this application help physicians make a more in-depth and accurate prediction of the disease progression of patients with primary liver cancer, thereby providing a useful reference for clinical treatment decisions.

The present disclosure provides methods of treating or preventing age-related diseases and disorders (e.g., age-related diseases or disorders associated with the glutamate pathway and / or glutaminase-1 (GLS1)) by administering to a subject in need thereof a provided compound (e.g., a compound of Formula (I)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. The present disclosure also provides methods of modulating mitochondrial function, reducing reactive oxygen species levels, reducing pro-inflammatory signaling, and / or preventing or inhibiting cellular senescence by contacting a cell, tissue, or biological sample with or administering to a subject in need thereof a provided compound, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof.

This invention discloses the application of bavachin in the preparation of drugs for alleviating and / or preventing senescence of uterine decidual stromal cells, belonging to the field of biomedical technology. Through drug library screening and experimental verification, this invention found that bavachin can significantly alleviate the senescent phenotype of human uterine decidual stromal cells, reduce the expression of senescence-related markers, and alleviate decidual stromal cell senescence by regulating intracellular copper ion metabolism and transport to maintain intracellular and extracellular copper ion homeostasis. This invention provides a novel drug target and intervention strategy for clinically improving endometrial decidual function and treating related reproductive health problems. This invention also provides the application of bavachin in the preparation of drugs for alleviating senescence of uterine decidual stromal cells.

This application discloses a method for preparing chitosan-derived carbon dots, the derived carbon dots themselves, and their applications. These carbon dots are prepared by amidation covalent coupling of octyl-citric acid chitosan-based amphiphilic polymer carbon dots and 2,3-epoxypropyltrimethylammonium chloride-modified lignin-based carbon dots. The octyl hydrophobic chain disrupts the hydrogen bond shielding of chitosan, exposing active sites and enhancing reactivity. Quaternization modification of the lignin-based carbon dots improves compatibility and imparts targeting properties. This achieves a triple synergistic anti-aging effect, scavenging reactive oxygen species, upregulating LaminB1 expression, and inhibiting IL-6 / IL-8 secretion. Cell experiments show that these carbon dots significantly reduce UVA-induced oxidative damage, increase hyaluronic acid synthesis, and reduce cellular senescence levels, with no significant cytotoxicity within effective concentrations. They show promising application prospects in the fields of antioxidants, skin photoaging protection, and anti-aging cosmetics and medical repair materials.

The present disclosure provides Pyruvate Dehydrogenase Kinase 4 (PDK4) as a target for intervention of cellular senescence and a use in chemotherapy against cancer. The present disclosure reveals PDK4 as a novel target for intervention of cellular senescence and intervention in drug resistance of tumors. By targeting PDK4, drugs can be developed to inhibit drug resistance of tumors, suppress or eliminate the SASP. Additionally, drugs targeting PDK4 can be used in combination with chemotherapeutic drugs for diagnosis or prognosis of related diseases or symptoms based on this target and mechanism.

The application discloses application of Biochanin A in preparation of a medicine for inhibiting or improving uterine decidua stromal cell senescence, and belongs to the field of biomedical technology. Through drug chemical library screening and experimental verification, it is found that Biochanin A can significantly alleviate the senescence phenotype of human uterine decidua stromal cells, reduce the expression of senescence-related markers, and alleviate decidua stromal cell senescence through regulation of mitochondrial energy metabolism. The application provides a brand-new drug target and intervention strategy for improving endometrial decidua function and treating related reproductive health problems in clinic, and provides application of Biochanin A in preparation of a medicine for alleviating uterine decidua stromal cell senescence.

Provided is a prophylactic and / or therapeutic agent for photodermatitis caused by light exposure. This prophylactic and / or therapeutic agent for a skin disorder caused by light exposure contains an inhibitor for cellular senescence-associated secretory phenotype factors (SASP factors) as an active ingredient. As a result of exploring responses to light exposure in melanocytes and comprehensively analyzing molecules that can be therapeutic target seeds related to the skin disorder, it was shown that cellular senescence occurs in melanocytes after light exposure. In melanocytes having undergone cellular senescence, enhanced expression of an SASP factor group was observed, and this led to the finding that an inhibitor for SASP factors is effective for preventing and / or treating the skin disorder.

The present invention relates to the technical field of biomedicine. The present invention aims to provide a use of Mn3O4 nanoparticles in alleviating intervertebral disc degeneration, trimanganese tetroxide nanoparticles Mn3O4 NPs are added as nanozymes to interventional drugs for treating intervertebral disc degeneration. The present invention uses Mn3O4 nanoparticles as nano-active catalytic enzymes, which have multi-enzyme catalytic activities similar to superoxide dismutase, catalase, and glutathione peroxidase, and can effectively scavenge reactive oxygen species (ROS) and control ECM metabolism, significantly reducing cell apoptosis, delaying cell senescence, inhibiting inflammation, and enhancing autophagy, thereby promoting annulus fibrosus AF repair in the treatment of intervertebral disc degeneration. Mn3O4 nanoparticles have good biocompatibility, and metabolites thereof can be used in other physiological processes, producing no toxic side effects in the in vivo circulation. Furthermore said nanoparticles perform stably in adverse microenvironments of low oxygen and low pH in intervertebral discs, and have in vivo stability that other active catalytic enzymes do not possess.

Among the various aspects of the present disclosure relates to methods and compositions useful in convert inflammatory dietary fatty acids (omega 6) to anti-inflammatory fatty acids (omega 3). Specifically, the present disclosure provides methods and compositions for increasing n-3 desaturase expression or activity in a subject. The disclosure provides various compositions for providing increased n-3 desaturase expression or activity including a variety of viral vector and engineered microorganisms. The disclosure provides, in part, methods for reducing local and / or systemic inflammation, improving wound healing, preventing premature cellular senescence, treating or preventing a disease, disorder, or condition related to inflammation or obesity and treating or preventing arthritis.

The present invention relates to functionally enhanced stem cells and a therapeutic composition comprising same and, more specifically, to functionally enhanced stem cells primed with a PRL-1 variant and a composition for treating metabolic diseases, comprising the functionally enhanced stem cells. According to the present invention, functionally enhanced mesenchymal stem cells can be obtained without artificial gene introduction, and the mesenchymal stem cells functionally enhanced according to the present invention exhibit increased cell growth and suppressed cellular senescence, thereby enabling the preparation of more effective stem cell therapeutics.

This invention discloses an extracellular vesicle miRNA novel-10 derived from fresh Polygonatum rhizome and its application in the preparation of anti-cellular senescence compositions, belonging to the field of extracellular vesicle miRNA technology. Using fresh Polygonatum rhizome as the source, this invention prepares extracellular vesicles using a tangential flow filtration system and detects multiple high-abundance miRNAs from the extracellular vesicles. Among them, miRNA novel-10, shown in SEQ ID No. 1, has a high expression abundance and can significantly reduce SA-β-gal positive levels in a bleomycin-induced MRC-5 cell senescence model, and can be used to prepare anti-cellular senescence compositions.

This invention discloses a method and its application for delaying cellular senescence in the in vitro expansion of mesenchymal stem cells. The method includes delaying the replicative senescence of human mesenchymal stem cells by inhibiting N-cadherin-mediated cell adhesion during in vitro expansion. Inhibition of N-cadherin-mediated cell adhesion includes adding inhibitors or reducing the expression level of genes encoding N-cadherin. The method of this invention can effectively reduce cell adhesion, restore the collective migration ability and traction of cells, and significantly downregulate the expression of aging-related markers p53 and p21, as well as SA-β-galactosidase activity. The method of this invention is simple to operate, low in cost, and can effectively improve the quality and yield of stem cell expansion.