41 results about "Atp production" patented technology

The invention provides electroactive nano short fibers for osteoarthritis cartilage repair and a preparation method thereof, the preparation method comprises the following steps: preparing a nano fiber membrane from a composite material of gelatin, polylactic acid and glycine crystals through electrostatic spinning, and preparing the obtained nano fiber membrane into short fibers; performing freeze drying on the short fibers, and then performing heating treatment to obtain a short fiber stent; the short fiber support is smashed and reacts with graphene oxide, modified graphene oxide short fibers are obtained, and then the modified graphene oxide short fibers are soaked in a mixed solution of alkaline dopamine and phosphatidylcholine for a reaction. The electroactive nano short fiber provided by the invention is low in friction coefficient, the expression quantity of Sirt1 in OA cartilage cells can be remarkably increased under ultrasonic stimulation, the ATP (adenosine triphosphate) productivity can be remarkably improved, release of inflammatory factors and degradation of extracellular matrixes can be inhibited, and meanwhile, a guarantee is provided for updating of a hydrated lubricating layer.

A pharmaceutical composition according to an aspect can be applied to the prevention, treatment or the like of endometrial damage, Asherman's syndrome, or complications thereof by: reducing the level of collagen accumulation in the endometrium; increasing the expression level of VEGF; increasing the expression level of Ki67; increasing the expression level of Itgb3; increasing the expression level of Spp1; increasing the number of implantation sites; decreasing the expression levels of fibrosis-related factors; decreasing the expression levels of metabolism-related factors; increasing ATP production; and regulating the expression levels of mitochondrial function-related factors.

The invention relates to a diatomic iron-iron site nano-enzyme constructed by relieving oxidative stress and cartilage degeneration and used for targeted osteoarthritis treatment. According to the invention, a nitrogen-doped porous carbon anchored diatomic iron nano enzyme catalyst (Fe2-NCs) with Fe-Fe dimer coordination is developed by using a'subject-object 'strategy. The Fe2-NCs protect cartilage cells from oxidative stress induced apoptosis by modulating ROS and active nitrogen species (RNS) and promoting O2 release. In addition, Fe2-NCs restores mitochondrial function by inhibiting NOX4 expression, improving ATP production, and normalizing COXIV levels. In an in-vivo OA model, the Fe2-NCs can reduce the expression of a pro-inflammatory medium COX-2 through an NF-kappa B signal channel, inhibit the up-regulation of MMP-13 and delay the degradation of type II collagen. The invention provides a new theoretical framework and methodological approach for the treatment of osteoarthritis, and has important clinical and scientific significance.

The invention discloses application of a mitochondrial differentiation expression gene in preparation of a depression diagnostic agent and a depression treatment drug, and relates to the technical field of depression diagnosis and treatment. And the mitochondrial differentiation expression gene comprises one or more of TFAM (Transforming Factor Amplification Molecular), SURF1 and NDUFB9. According to the present invention, the SURF1 gene simultaneously expressed in inhibitory neurons and excitatory neurons is focused on, the key effect of the SURF1 in CUMS-induced depression-like behaviors is found, the CUMS-induced molecular and behavior changes are effectively reversed by the overexpression of the SURF1, and the potential anti-depression effect is displayed; besides, animal experiments find that overexpression of the SURF1 can effectively recover the function of an electron transport chain, ATP generation is enhanced, mitochondrial membrane potential is maintained, and oxidative stress is reduced. The effects jointly relieve depression-like behaviors induced by CUMS, and further support the protection effect of the SURF1 in a depression model, which provides evidence for the new effect of the SURF1 in the pathophysiology of depression.

The present invention provides a human T cell lacking human leukocyte antigen (HLA) class I molecule and containing an exogenous ST6GALNAC6 gene, which has the following characteristics (a) and / or (b):(a) CD62L-positive and CD45RA-positive(b) a total ATP production rate of a human T cell-containing cell population of 400 pmol / min / 105 cells or more and a mitochondrial spare respiratory capacity of 40 pmol / min / 105 cells or more, 5-6 days after the application of T cell proliferation stimulation to the cell population. According to the present invention, a low-immunogenic human T cell that can remain stably in the body for a long period of time after transplantation is provided, and the development of a versatile CAR-T cell or TCR-T cell for allotransplantation becomes possible by using the human T cell.

To provide agents for promoting epidermal keratinocyte growth, filaggrin mRNA expression, serine palmitoyltransferase mRNA expression, involucrin expression or ATP production by finding substances having excellent activity in promoting epidermal keratinocyte growth, filaggrin mRNA expression, serine palmitoyltransferase mRNA expression, involucrin expression or ATP production.SOLUTION: An epidermal keratinocyte growth promoting agent of the invention comprises one or more effective ingredients selected from the group consisting of 2-ketoglutaric acid, 2-isopropyl malate, inosine 5'-monophosphoric acid, succinic acid, malic acid and pyruvic acid. Also, a filaggrin mRNA expression promotor, a serine palmitoyltransferase mRNA expression promotor, an involucrin expression promotor of the invention comprise, as an effective ingredient, 2-ketoglutaric acid. Further an ATP production promotor of the invention comprises 2-isopropyl malate as an effective ingredient.SELECTED DRAWING: None

This invention relates to the field of cosmetic compositions, and more specifically to a synergistic anti-aging composition involving energy metabolism and autophagy, its preparation method, and its application. The composition comprises sea buckthorn fruit extract, trehalose, and a cosmetically acceptable polyol carrier. This invention pioneers a betaine-trehalose-NADES extraction system, achieving low-temperature, high-efficiency extraction while preserving the heat-sensitive active ingredients of sea buckthorn. Trehalose possesses both extraction and autophagy activation effects. A selective separation strategy achieves a balance between efficacy, compliance, and process simplicity. The green, circular process reduces costs and is environmentally friendly. Through the synergistic effect of sea buckthorn fruit extract and trehalose, the composition enhances mitochondrial membrane potential, increases ATP production, inhibits excessive activation of the mTOR pathway, and promotes LC3-II conversion, thus synergistically combating skin aging from multiple targets including cellular energy metabolism, signaling pathways, and autophagy.

To provide a composition capable of improving skin vitality reduced by stress.SOLUTION: A composition disclosed herein includes a thymol ester-based compound as an active ingredient, thereby promoting ATP production through mitochondrial activity and further restoring the vitality of skin cells reduced due to stress.SELECTED DRAWING: Figure 2

A micronutrient composition comprises of several combinations of individual ingredients in forming Mix 11, G12, G13 and core mix formulation. Core mix contains magnesium citrate, alpha-Ketoglutaric acid, L-Citrulline and Taurine. The Mix 11, G12 and G13 contains Magnesium Citrate, Alpha-Ketoglutaric Acid, Niacinamide, L-Glutamine, L-Citrulline, Sodium Pyruvate, Succinic acid, Vitamin B complex, Taurine, L-Cysteine, L-Methionine, L-Ascorbic Acid, Coenzyme Q10 or combination thereof. A method of administering and treating a specific disease which is due to one of an oxidative stress, impaired mitobiogenesis and ATP production in a mammal is disclosed.

The present invention relates to a method and system for producing adenosine triphosphate (ATP) through an acid / aldehyde-ATP (AAA) cycle in an electrochemical cell.

The invention discloses a method for improving the yield of L-threonine by enhancing Escherichia coli electronic respiration transfer and energy transfer efficiency, and belongs to the technical field of genetic engineering. According to the invention, a cytochrome bo oxidase subunit CyoA mutant derived from escherichia coli, a cytochrome bo oxidase subunit CyoB mutant derived from pseudomonas aeruginosa, a cytochrome bd oxidase cydAB gene cluster derived from escherichia coli and a polyphosphate kinase PPK mutant derived from radiation-resistant coccus are introduced, amn genes are knocked out, and a cytochrome bo oxidase gene is obtained. The electron transfer efficiency in escherichia coli and the production efficiency of energy ATP (adenosine triphosphate) are enhanced, and the production efficiency of L-threonine and the carbon yield are further improved. Finally, the obtained engineering strain ECTHRS-5 is subjected to fed-batch fermentation in a 5L fermentation tank to accumulate 160.8 g / L of L-threonine, and the sugar-acid conversion rate is 0.62 g / g.

The present invention provides a biomimetic liposome nanoreactor, a preparation method and its application, and relates to the field of biomedical engineering technology. The biomimetic liposome nanoreactor comprises liposomes, thylakoid membrane fragments and electron donors. The present invention integrates thylakoid fragments (Tk) into liposomes (Lip) and loads electron donors into the liposomes to prepare a biomimetic liposome nanoreactor. The biomimetic liposome nanoreactor of the present invention can be taken up by renal epithelial cells and catalyze NAD + Generate; and under the drive of ultrasound, the electron transport chain on it transfers a large number of electrons to the cytoplasm, converting NAD + Reduction to NADH promotes ATP production, rapidly alleviating AKI in the early stages. Furthermore, in the presence of electrons, the effective generation of NADPH fundamentally prevents the generation of oxidative stress such as ROS, effectively preventing the progression of AKI to CKD.

The present invention relates to a method for activating the mitochondrion, wherein mainly negative charges and reactive oxygen species are supplied to the mitochondrion from the outside via a negative charge and reactive oxygen species delivery unit to serve as material for the mitochondrial redox reaction. A calcium ion channel stimulation unit stimulates an in vivo calcium ion to transport the protein across the calcium on the inner mitochondrial membrane into a mitochondrial matrix space, such that the influx of calcium ions promotes mitochondrial depolarization and increases the activity of mitochondrial oxidative phosphorylation. This enhances mitochondrial activation and ATP production.

The present invention relates to the control and enhancement of energy production of mitochondria through maximizing electron transfer efficiency using natural pigments and light. The composition for mitochondrial modification according to the present invention, which comprises two or more natural pigments selected from the group consisting of □-carotene, anthocyanin, and chlorophyll a as active ingredients, and the mitochondria modified by mixing these active ingredients have the effects of increasing ATP production and decreasing ROS production, and thus can be usefully used as a health functional food composition for improving exercise function and fatigue. Moreover, the effect of promoting the production of mitochondrial energy and preventing oxidative damage by light irradiation, can be used for the prevention and treatment of diseases related to mitochondrial dysfunction.

The invention discloses an application of mitochondrial glutamate transporter SLC25A22 in treatment of Parkinson's disease, and provides an application of SLC25A22 as a target in screening of drugs for treatment of Parkinson's disease and an application of a preparation for promoting expression of SLC25A22 in preparation of drugs for treatment of Parkinson's disease. Research finds that SLC25A22 promotes utilization of glutamic acid in MN9D cell mitochondria, synthesis of alpha-ketoglutaric acid and TCA circulation, and improves generation reduction of ATP in MN9D cells induced by MPP +, ROS accumulation and mitochondrial membrane potential decline, so that damage of MN9D cell activity is relieved, and finally loss of dopaminergic neurons is rescued.

The invention belongs to the technical field of biological medicines, and particularly discloses a polypeptide for protecting lung vascular endothelial cells and relieving lung injury and application of the polypeptide. The polypeptide is Humanin-G (HNG), and the amino acid sequence of the polypeptide is MAPRGFSCLLLLTGEIDLPVKRRA. The polypeptide is targeted to mitochondria of pulmonary vascular endothelial cells, provides protection from energy supply and cell survival roots, and has profound significance in improving functions of the pulmonary vascular endothelial cells and reducing the death rate of sepsis-induced acute lung injury (ALI). Researches show that when the polypeptide is used in the acute injury stage, lung inflammation of a model animal can be relieved by 25%-50%, the lung injury HE score can be reduced by about 50%, pulmonary edema can be relieved by about 30%, mitochondrial functions can be recovered by about 70%, the ATP yield can be increased by 30%, and the effect is excellent. Therefore, the invention provides a brand new strategy for maintaining the mitochondrial homeostasis by using the polypeptide so as to relieve lung injury.

This invention relates to a mitochondrial composite nanosystem DTPS@Mito targeting lung inflammation, comprising a mitochondrial core and a functionalized lipid material DSPE-TK-PEG2000-SA modified on its surface. DSPE acts as a hydrophobic anchor inserted into the mitochondrial outer membrane, PEG2000 provides hydrophilicity and biocompatibility, ketithiothiol bonds serve as ROS-responsive linkers, and sialic acid targets the head group to specifically bind to E-selectin, which is highly expressed at the inflammatory site. The DTPS@Mito particles have a diameter of approximately 832 nm, maintaining intact mitochondrial morphology and protein composition. In vitro experiments show that it significantly inhibits the expression of inflammatory factors, reduces ROS levels, restores ATP production, and regulates mitochondrial dynamics. In vivo experiments show that it has enhanced retention and accumulation capacity in the lungs of ARDS mice, significantly alleviating lung inflammation, tissue damage, and oxidative stress, and reducing hyaline membrane formation. This invention achieves the synergistic integration of three major functions: mitochondrial transplantation, targeted delivery, and antioxidation, and can be used to prepare drugs for the treatment of acute respiratory distress syndrome.

This invention relates to the field of cell biology, and discloses a culture medium and method for inducing physiological myocardial hypertrophy based on carnosine. The culture medium for inducing physiological myocardial hypertrophy contains carnosine. By introducing an appropriate concentration of carnosine into a cardiomyocyte system, this invention can induce a series of phenotypic changes in cardiomyocytes related to physiological myocardial hypertrophy, including increased cardiomyocyte area, increased mitochondrial number, enhanced oxidative metabolic capacity, and increased ATP production capacity. These changes can improve the energy metabolism level of cardiomyocytes, thus providing a new technical solution for studying myocardial adaptive remodeling.

This invention relates to the field of cell culture technology, and discloses a method for culturing NK cells and its applications. When NK cells enter a hypoxic environment, not only do their cytotoxic activity and proliferative capacity rapidly decline, but they also experience metabolic disorders such as impaired mitochondrial function, insufficient ATP production, and abnormal accumulation of reactive oxygen species (ROS), leading to functional failure and limiting their application in tumor therapy. Existing technologies mainly rely on constant or single-stage hypoxia induction, failing to improve the insufficient hypoxia adaptation of NK cells at the metabolic level. Therefore, this invention provides a method that uses repeated acclimatization culture with gradually decreasing oxygen concentration to allow NK cells to gradually adapt to the metabolic demands of a hypoxic environment. NK cells cultured using this method exhibit a more stable metabolic state and superior cytotoxic activity in a hypoxic environment, significantly enhancing their anti-tumor efficacy and solving the problem of metabolic imbalance and rapid functional loss of NK cells in the hypoxic tumor microenvironment in existing technologies.

The present application relates to a novel micropeptide MP29 and a use thereof and relates to a use of the micropeptide in the preparation of a reagent or drug for preventing, treating, or alleviating diseases related to abnormal mitochondrial energy metabolism in cells, wherein the diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, schizophrenia, aging, photoaging, fatty liver disease, liver fibrosis, liver cirrhosis, liver cancer, diabetic nephropathy, cardiovascular diseases such as heart failure, etc. By means of endogenous overexpression or exogenous synthesis, the reducing equivalents NADH in the tricarboxylic acid cycle are up-regulated to promote intracellular ATP production, thereby significantly enhancing the proliferation of high-energy-demanding cardiac cells and brain tissue cells, or suppressing oxidative damage and apoptosis of cells in Alzheimer's disease models and Parkinsonism, or alleviating hypertrophy and aging of myocardial cells in heart failure models, or ameliorating the photodamage of cells in photoaging models. These results indicate that the micropeptide MP29 has an application value in preventing or treating diseases related to abnormal mitochondrial energy metabolism.

The present invention relates to a method and system for producing adenosine triphosphate (ATP) through an acid / aldehyde-ATP (AAA) cycle in an electrochemical cell.

The invention discloses a method for establishing an oligoasthenospermia animal model by utilizing flunarizine and application of the method, and belongs to the technical field of biological medicines. The method comprises the following steps: randomly grouping SPF-level experimental animals; injecting a flunarizine FNZ solution into the abdominal cavity continuously for 7 days; and verifying the oligospermia and asthenozoospermia indexes. In the animal model constructed by the method, the number and activity of sperms in the epididymis of an experimental animal are reduced, the mitochondrial membrane potential of the sperms is reduced due to FNZ, and ATP production is reduced, which indicates that the FNZ reduces the quality of the sperms. Therefore, the method for constructing the oligoasthenospermia model provides a proper animal model for researching male infertility diseases such as oligoasthenospermia and the like; the animal model can be used for animal experiments and new drug research and development for researching and developing occurrence and development mechanisms of male infertility diseases.

HTS screening was performed regarding cell proliferation, one of symptoms of senescence. As a result, KB1541, which was the most effective on cell proliferation, was earned. The present invention described how the compound regulates cell proliferation and senescence. The present invention uncovered what proteins interacted with the compound using streptavidin-magnetic beads after treating with biotin-connected KB1541. Consequently, it was identified that mitochondrial proteins interacted with the compound. In ATP assay, electron microscope and IP assay, the inventors identified that the compound regulated mitochondrial proteins and thereby increased ATP production as well as recovered senescence.

A use of a ramie extract in preparing a composition for anti-aging is provided. The composition containing ramie extract can improve the function and activity of mitochondria and telomerase and protect mitochondria from oxidative stress, including decrease in the proton leakage, increase in the ATP production, increase in the spare respiratory capacity, increase in the maximal respiratory capacity, or increase in the ATP coupling efficiency.

This invention discloses the application of NT5C1A as a therapeutic target for myocardial ischemia-reperfusion injury, belonging to the field of biomedical technology. Through proteomics screening and in vitro and in vivo experiments, this invention is the first to discover and demonstrate that NT5C1A is upregulated in the pathological process of MIRI, and is a key upstream factor regulating the AMPK / SIRT1 / PGC-1α signaling pathway. Overexpression of NT5C1A can effectively activate this pathway, synergistically regulating multiple downstream pathological processes: promoting the expression of mitochondrial fusion proteins Mfn-2 and OPA1, inhibiting the expression of the splitting protein DRP1; significantly promoting ATP production and improving energy metabolism disorders; and regulating the balance of apoptosis-related protein Bax / Bcl-2 expression, inhibiting cardiomyocyte apoptosis, ultimately reducing myocardial damage, improving myocardial function, and reducing the infarct area. This invention provides a new target and strategy for the precise intervention of MIRI.

Provided are therapeutic methods and pharmaceutical preparations configured to treat primary and secondary mitochondrial dysfunction. The methods and treatments use agonists of AMPK. The agonists activate AMPK to activate ATP production pathways and inhibit ATP consumption pathways, thereby allowing for the alleviation of symptoms associated with mitochondrial dysfunction.

The application discloses a polyphosphate kinase and application thereof in improving ATP production, and belongs to the technical field of genetic engineering.The polyphosphate kinase disclosed by the application is PePPK, PsPPK, RbPPK or RrPPK, and the amino acid sequence is shown as SEQ ID NO.5-8.The polyphosphate kinase disclosed by the application can improve ATP production, and can synthesize glutathione and 3'-phosphoadenosine-5'-phosphosulfate.

The invention provides a method for increasing the number and activity of cell mitochondria by using leonurine. The method comprises the following steps: (1) selecting active ingredients; (2) processing concentration and time windows; (3) suitable cell types; and (4) detecting indexes and verifying a system. The number and activity of mitochondria are improved, after leonurine treatment, the number of cell mitochondria is increased, the mitochondrial membrane potential rises, the ATP generation level is improved, and the oxygen consumption rate is increased. According to the invention, the oxidative stress tolerance of the cells is enhanced, the treated cells are exposed in an anoxic (such as 0.1% oxygen) or oxidative stress environment, and the cell survival rate and function are obviously better than those of an untreated group.

This invention relates to the field of biomedical technology, and more particularly to the use of a combination of RVX208 and temozolomide for the treatment of glioblastoma. It also relates to the use of RVX208 to resensitize temozolomide-resistant cancers to temozolomide treatment. The use of at least one of RVX208, a pharmaceutically acceptable salt of RVX208, a solvate of RVX208, a hydrate of RVX208, a polymorph of RVX208, an isomer of RVX208, a prodrug form of RVX208, and temozolomide in the preparation of a glioblastoma therapeutic agent. RVX208 inhibits the transcriptional activity of various genes related to cell cycle progression and proliferation maintenance by inhibiting BET family proteins or other target molecules, leading to cell cycle arrest, inhibition of cell proliferation, and induction of programmed cell death. RVX208 also interferes with the transcriptional expression of genes related to mitochondrial homeostasis regulation, resulting in a decrease in mitochondrial membrane potential and reduced ATP production, thus enabling RVX208 to disrupt mitochondrial function in GBM cells and produce a synergistic antitumor effect with temozolomide.

The invention discloses polyphosphate kinase and application thereof in increasing ATP (adenosine triphosphate) output, and belongs to the technical field of gene engineering. The polyphosphate kinase disclosed by the invention is PePPK, PsPPK, RbPPK or RrPPK, and the amino acid sequence of the polyphosphate kinase is as shown in SEQ ID NO. 5-8. The polyphosphokinase disclosed by the invention can be used for increasing the generation amount of ATP (adenosine triphosphate) and synthesizing glutathione and 3 '-phosphoadenosine-5'-phosphoryl sulfuric acid.