184 results about "Mitochondrion membrane" patented technology

The invention belongs to the technical field of bioengineering, and discloses a sunflower seed peptide for regulating metabolism of brain cells, the sunflower seed peptide has a biological sequence of Arg His Ala Lys Thr Pro Ser Asn Lys, and a preparation method of the sunflower seed peptide for regulating metabolism of brain cells comprises the following specific steps: S1, raw material pretreatment; s2, peeling and crushing; s3, protein extraction; s4, performing enzymolysis treatment; s5, performing enzyme deactivation treatment; s6, filtering and purifying; s7, concentrating and drying; and S8, quality detection and packaging. The sunflower seed protein is directionally decomposed into the active peptide fragment by precisely regulating and controlling compound protease and enzymolysis conditions, the active peptide fragment can be compatible with a brain cell specific receptor and penetrate through a blood brain barrier, and cell experiments and animal models prove that the peptide fragment can activate a mitochondrial respiratory chain complex, so that the mitochondrial membrane potential is increased by more than 30%, and the mitochondrial membrane potential is increased by more than 30%. Meanwhile, the activity of neurotransmitter synthetase can be enhanced, the brain health is protected, and tests further prove that the sunflower seed peptide also has the function of regulating the metabolism of brain cells.

The invention relates to the technical field of antitumor drugs, in particular to a Ru (II) complex and a preparation method and application thereof, and the Ru (II) complex has a structure as shown in a formula I. The Ru (II) complex synthesized by the method disclosed by the invention not only has relatively high cytotoxicity, but also has good photodynamic antitumor activity. After the complex is illuminated, the efficiency of the complex entering cells in an active transportation mode can be accelerated, mitochondria and endoplasmic reticulum are targeted at the same time, mitochondrial membrane potential decline and endoplasmic reticulum stress are caused to form a dual organelle damage effect, immunogenic cell death is caused, the tumor microenvironment is adjusted, and the tumor cell immunogenicity is improved. The enrichment of dendritic cells (DCs) in tumor cells is realized, the chemotactic activity of effector T cells is improved, the proportion of CD4 < + > and Foxp3 < + > cell populations is reduced, and finally the anti-tumor immune response is activated. Meanwhile, the complex provided by the invention can also induce the cell to generate pan apoptosis, retard the cell cycle in the G2 / M period and enhance the effect of the complex in inhibiting tumor proliferation.

The invention belongs to the technical field of cosmetics, and discloses a composition for promoting metabolism of hair papilla cells as well as a preparation method and application of the composition. The composition disclosed by the invention is prepared from the following components: a cacumen biotae extract, trehalose, betaine, acetyl tetrapeptide-3 and myristoyl pentapeptide-4. The components in the composition have a good synergistic effect, the mitochondrial membrane potential of the hair papilla cells can be obviously enhanced, the cell activity of the hair papilla cells is promoted, the cell metabolism function of the hair papilla cells is promoted, and therefore the health of hair follicles is effectively maintained.

The invention discloses a modular tumor microenvironment response polypeptide and a preparation method and application thereof. The modular tumor microenvironment response polypeptide is composed of the following functional modules: a targeting and chemotactic module used for targeting tumor cell surface p32 protein and tumor lymphatic vessels and promoting tumor tissue penetration and enrichment; the microenvironment double-response module is used for being cut by MMP-2 / 9 enzyme and broken by high-concentration glutathione GSH in a tumor microenvironment to trigger self-assembly; the self-assembly driving module is used for exposing after the microenvironment responds to activation and driving short peptides to be self-assembled to form a nano structure; a killing module: a pro-apoptotic peptide PAD used for targeting a mitochondrial membrane and inducing tumor cell apoptosis; and the stability optimization module is used for enhancing the degradation resistance of the oligopeptide. By integrating targeted delivery, enzyme digestion response, acid-sensitive release and stabilizing structures, the problems of insufficient targeting property, inaccurate release, poor stability, diagnosis-treatment splitting and the like of the anti-tumor drug and the developing agent are solved.

[Problem] It is an objective of the present invention to provide an enhancer with useful actions such as increase action of cardiolipin molecular species as a component of an inner mitochondrial membrane including 3,5-dihydroxy-4-methoxybenzyl alcohol as an active ingredient. [Solution] The present invention features the increase action of cardiolipin molecular species as a component of an inner mitochondrial membrane including 3,5-dihydroxy-4-methoxybenzyl alcohol as an active ingredient.

The invention discloses a nasal delivery multistage targeting bionic nano drug delivery system as well as a preparation method and application of the nasal delivery multistage targeting bionic nano drug delivery system. According to the drug delivery system, a black phosphorus nanosheet with an active oxygen scavenging effect is used as an inner core carrier, a neuroprotective agent fingolimod hydrochloride FTY720 and polydimethyldiguanide PolyMet are loaded, and a microcolloid cell membrane and a mitochondrial membrane are modified on the surface of the preparation; the nano drug delivery system is applied to treatment of cerebral arterial thrombosis reperfusion injury, can overcome the blood brain barrier, can quickly enter the brain through nasal administration, realizes efficient delivery of drugs, remarkably reduces the cerebral infarction area, reduces the brain inflammation level, protects nerve cells, greatly relieves cerebral arterial thrombosis reperfusion injury, and has application prospects.

The invention relates to a mitochondrial uncoupling inhibitor sustained-release nanodot, a preparation method thereof and application of the nanodot in type 2 diabetes mellitus, and belongs to the technical field of nano-drugs. According to the preparation method disclosed by the invention, glycine and genipin are subjected to Schiff reaction to prepare the slow-release nanodot, and the slow-release nanodot is of a monodisperse spherical structure, has surface negative charges, and can slowly release genipin under physiological conditions, so that the mitochondrial protection effect of the genipin is fully exerted. The mitochondrial uncoupling inhibitor slow-release nanodot prepared by the invention can obviously improve the mitochondrial membrane potential, increase the cell ATP content, effectively inhibit mtDNA release under the stimulation of IL-1beta and palmitic acid, effectively inhibit STING inflammation pathway activation under the stimulation of IL-1beta and PA, obviously reduce pancreatic beta cell apoptosis, obviously relieve endoplasmic reticulum stress, and can be used for preparing the mitochondrial uncoupling inhibitor slow-release nanodot. The T2DM mouse blood sugar is obviously reduced, the glucose tolerance dose and the insulin sensitivity are improved, and good biocompatibility is achieved.

The invention provides a genetically engineered oriented electrostatic spinning fiber as well as a preparation method and application thereof, and belongs to the technical field of biomedical materials. Gene TSPAN9 is packaged in liposome through a micro-fluidic chip technology, then oriented electrostatic spinning fibers of a shell-core structure are prepared through an oriented micro-sol electrostatic spinning technology, and the liposome containing the TSPAN9 is protected on a core layer by hyaluronic acid; and the polylactic acid fibers are arranged in an oriented manner to form a shell layer. An in-vitro experiment shows that the oriented fiber closely simulates a fascia oriented arrangement structure, and the cell migration rate is remarkably improved through contact guidance; by slowly releasing lipidosome loaded with genes into cells and maintaining the mitochondrial steady state, mitochondrial respiration is effectively recovered, the active oxygen level is reduced, and the mitochondrial membrane potential function is maintained. In-vivo experiments show that the genetically engineered fiber can effectively inhibit inflammatory response and promote fascia tissue regeneration by promoting mitochondrial exocytosis to discharge damaged mitochondria.

The invention discloses an acoustic catalyst as well as a preparation method and application thereof, and belongs to the technical field of catalysts and drug therapy. NJU-319 is selected as an acoustic catalyst, NJU-319Pt is synthesized from a porphyrinyl linker (TAPP) and a hexaphenyl triphenyl unit (HFPTP) under a solvothermal condition, and the H2 generation efficiency of NJU-319Pt can be further improved. After intraperitoneal injection, the nano-drug NJU-319Pt catalyzes H2O to be reduced into H2 under ultrasonic irradiation, and meanwhile lactic acid is oxidized into pyruvic acid. The action mechanism comprises: removing ROS and relieving oxidative stress; by inhibiting an NF-kappa B pathway, the transformation of macrophages from M1 phenotype to M2 phenotype is promoted, and inflammation is reduced; mitochondrial membrane potential is reduced, EMs cell apoptosis is induced, and focus growth is inhibited. The research provides a brand new EMs treatment strategy, combines acoustic catalysis H2 generation with lactic acid oxidation, and provides a new direction for EMs treatment research.

The invention provides a novel application of a raspberry extract. It is found through tests that any one of isoquercitrin, ellagic acid, vanillic acid, oleanolic acid, kaempferol-3-O-rutinoside, kaempferol-3-O-sophoroside, tiliroside, tormentic acid and raspberry extract can remarkably improve the activity of the human ovarian granular cells or remarkably improve the oxidative stress level, and the activity of the human ovarian granular cells can be remarkably improved. According to the present invention, the ovarian function can be effectively protected by the eight components, the ovarian function can be effectively protected by the eight components, or the mitochondrial membrane potential level can be significantly regulated and controlled, or the estrogen level in the microenvironment can be effectively maintained, such that the ovarian function can be effectively protected by the eight components, and the raspberry extract containing the eight components. The invention provides a new choice for ovarian function protection products, and also provides a new application for the substances.

The invention relates to the technical field of biological medicines, and particularly discloses application of betaine in preparation of a medicine for preventing or treating sepsis myocardial injury. Betaine (BET) provided by the invention can be used for effectively relieving cytokine storm caused by sepsis injury and inhibiting reduction of core body temperature of a mouse; the abnormal blood routine and blood biochemical indexes are improved. In addition, betaine can reduce generation of active oxygen in myocardial cells of the HL-1 mouse and improve mitochondrial membrane potential imbalance of the myocardial cells of the HL-1 mouse. The chemical structural formula of the betaine is shown in the specification.

The invention discloses application of fraxinellone as a cGAS-STING signal channel inhibitor in preparation of a medicine for treating inflammatory bowel disease, and belongs to the technical field of biological medicine. Aiming at the problem that the specific action mechanism between fraxinellone and the inflammatory bowel disease is not clear, the invention researches the specific action mechanism of fraxinellone for exerting the treatment and protection effects on the inflammatory bowel disease from the in-vivo and in-vitro aspects. Results show that the FRA can significantly inhibit the increase of the ROS level of IEC-6 cells caused by LPS, improve the mitochondrial membrane potential, significantly improve the pathological characteristics of DSS-induced mouse weight loss, DAI index increase, red, swollen and shortened colon, damaged colon tissue structure and the like, and inhibit the expression level of inflammatory factors. According to the present invention, it is found that the FRA can up-regulate the TJ tight junction protein and recover the intestinal barrier function by regulating the expression of cGAS-STING signal channel related proteins such as cGAS, STING, p-TBK1, NF-kappa B and the transcriptional level of mRNA, such that the IBD treatment effect is provided, and the basic basis is provided for the development of the new IBD treatment drug or strategy.

The invention discloses a preparation method of DRP1 engineered mitochondrial derived vesicles and application of the DRP1 engineered mitochondrial derived vesicles in cell aging resistance. The method comprises the following steps: firstly, constructing a lentiviral vector of an overexpressed DRP1 gene, and transfecting cells to obtain a cell strain of the stable overexpressed DRP1 gene; and culturing the cell strain, collecting a culture solution, and separating and extracting the mitochondrial derived vesicles to obtain the DRP1 engineered mitochondrial derived vesicles DRP1-MDVs rich in mtDNA. The DRP1-MDVs is used for treating senescent cells, the DRP1-MDVs is successfully internalized into senescent cells, the ROS level can be effectively reduced, the mitochondrial mtDNA and ATP content can be improved, the mtDNA mutation rate can be reduced, the mitochondrial membrane potential and the mitochondrial network structure can be recovered, and finally the expression of senescence-related proteins P16 and P21 can be reduced. The obvious mitochondrial function repairing potential and the cell aging improving effect are shown.

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.

The invention discloses a nanocomposite HA / PEI / Fe3O4 (at) siRNA and a preparation method and application thereof, and belongs to the technical field of antitumor drugs. The nano-composite HA / PEI / Fe3O4 coated siGPX4 is successfully prepared, the serum stability is high, the blood compatibility is good, siGPX4 can be efficiently released when the nano-composite reaches a tumor acidic microenvironment, then the anti-tumor effect is exerted, triple negative breast cancer cells can be specifically targeted, the internalization ability of MDA-MB-468 cells on the nano-composite is greatly improved, and the delivery efficiency of siGPX4 is remarkably improved; in the presence of H2O2, the nano-composite can down-regulate expression of GPX4, released ferrous ions and H2O2 are subjected to Fenton reaction, ROS in cells is remarkably increased, mitochondrial membrane potential is reduced, ferroptosis is triggered, MDA-MB-468 cell proliferation is remarkably inhibited, and the anti-tumor effect is achieved.

The invention provides application of taurochenodeoxycholic acid in preparation of a medicine for preventing and / or treating Fuchs corneal endothelial dystrophy, and particularly belongs to the technical field of medicine preparation. The invention provides an application of taurochenodeoxycholic acid in preparation of a medicine for preventing and / or treating Fuchs corneal endothelial dystrophy. Test results show that taurochenodeoxycholic acid can realize prevention and / or treatment of corneal endothelial cell injury caused by UVA; the number reduction, activity reduction, oxidative stress, ROS level rise and mitochondrial membrane potential drop of corneal endothelial cells caused by UVA are relieved; mitochondrial biological energy deficiency caused by UVA is relieved; and the prevention and / or treatment of the Fuchs corneal endothelial dystrophy are / is realized by activating a Ca < 2 + > signal channel.

The invention relates to a composition for regulating autophagy of eukaryotic cells and improving mitochondrial dysfunction as well as a preparation method and application of the composition. Comprising the following raw materials in parts by weight: 10-30 parts of broccoli powder, 10-30 parts of wheat germ microcapsule powder, 20-40 parts of raspberry extract, 20-40 parts of banana powder, 2-6 parts of leucine and 0.1-1 part of pyrroloquinoline quinone disodium salt. The invention further provides a preparation method of the broccoli powder, the wheat germ micro-capsule powder, the raspberry extract and the banana powder, and application of the composition of the broccoli powder, the wheat germ micro-capsule powder, the raspberry extract and the banana powder. The composition integrates the effects of the six components, is reasonable in compatibility, safe and effective, and various components activate mitochondria by regulating protein and depending on a PINK1 / Parkin dependent pathway and a PINK1 / Parkin non-dependent pathway; meanwhile, by activating a PGC-1alpha signal channel, mitochondrial DNA replication and new mitochondrial generation are promoted; the mitochondrial membrane potential is stabilized, and the ATP synthesis efficiency is improved; mitochondrial autophagy is synergistically activated, mitochondrial dysfunction is improved, and aging is relieved.

The invention discloses a preparation method of a high-activity mitochondrial targeting MAPS polypeptide preparation, and relates to the technical field of biologication.The preparation method comprises the steps of S1, polypeptide design and synthesis, S2, thiol oriented cross-linking, S3, cutting and purification, S4, liposome assembly and S5, freeze-drying preparation molding.The preparation method has the advantages that by designing an amphipathic alpha-spiral polypeptide structure, the high-activity mitochondrial targeting MAPS polypeptide preparation is obtained; a stable helical conformation is spontaneously formed in a physiological environment by utilizing the alternative arrangement characteristic of hydrophobic and hydrophilic residues; the hydrophobic surface of the conformation can effectively interact with the mitochondrial membrane lipid bilayer, so that the transmembrane resistance is reduced; meanwhile, the hydrophilic surface is combined with the high negative membrane potential of the mitochondrial inner membrane through charge interaction to form a directional driving effect, so that the active transfer efficiency of the polypeptide under the mitochondrial membrane potential is remarkably improved; in addition, the integrated mitochondrial positioning signal further specifically recognizes the mitochondrial outer membrane transporter, the polypeptide is assisted to be accurately anchored to the targeting site, and non-specific diffusion is reduced.

The invention discloses a protein complex for protecting mitochondria from being damaged, a pharmaceutical composition and application. According to the application, the influence of nitrate on mitochondrial injury in in-vivo radiation-induced salivary gland injury and in-vitro human salivary gland cell injury is evaluated, the action mechanism in the mitochondrial injury is further deeply explored, and a result shows that sialic acid transporter interacts with FKBP8, so that the mitochondrial injury can be inhibited, and the mitochondrial injury can be inhibited. In turn, particles are formed and anchored on the outer mitochondrial membrane, thereby maintaining membrane integrity. Therefore, the invention provides a brand new therapeutic target for preventing radiation-induced salivary gland injury and other mitochondrial membrane related diseases.

The disclosure provides a hybrid membrane camouflaged nanomedicine loaded with oxidative phosphorylation inhibitor and preparation method thereof. The nanomedicine comprises an inner core and an outer shell coated on the periphery of the inner core. The inner core is a ROS-responsive drug-loaded nanoparticle, and the drug loaded by the ROS-responsive nanocarrier is an oxidative phosphorylation inhibitor. The outer shell is a hybrid membrane of mitochondrial membrane and cancer cell membrane. The nanomedicines can cross the BBB and reach tumor sites by the homologous targeting of cancer cell membrane, and then they can homologously target and enter mitochondria by the mitochondrial membrane. Subsequently, under the high-level ROS environment of the mitochondria, the ROS responsive drug-loaded nanoparticle releases the oxidative phosphorylation inhibitor due to the swell and degradation of the inner core, so that the safe and efficient targeted GBM therapy is achieved.

The invention discloses an application of a vinyl quinoline fluorescent dye in preparation of a reagent or a kit for detecting mitochondria or lysosome. The fluorescent dye does not need to be washed, the probe is used for dyeing mitochondria when the mitochondrial membrane potential is normal, and the probe targets lysosome when the mitochondrial membrane potential is reduced, so that the probe can also be used for observing the mitochondrial membrane potential, the influence of washing on the mitochondrial membrane potential and the damage to cells can be avoided, and the applicability is wider.

The present invention belongs to the field of molecular biology, and particularly relates to a mutant and a mutant plasmid of an FUNDC1 gene, and a construction method therefor and the use thereof. The provided mutant plasmid has an increased FUNDC1 protein expression level, and can increase the protein expression level of mitophagy proteins COXⅣ and TOM20. After the transfection of the mutant plasmid, the cell activity and mitochondrial membrane potential are not significantly changed, indicating that the mutant plasmid can inhibit mitophagy and causes no damage to mitochondria, which provides a feasible solution for the preparation of a mitophagy drug, and has great significance for the research on the pathophysiological mechanism of myocardial I / R injuries.

The application discloses a tumor-penetrating carrier-free nanomedicine as well as a preparation method and application thereof, and belongs to the field of nanomedicine. The carrier-free nanomedicine can significantly improve water solubility of a water-insoluble compound, has mitochondrion targeting and tumor active penetration capabilities, and under the action of a tertiary amine nitrogen oxygen group, the carrier-free nanomedicine can be mostly transported into mitochondria, which is beneficial to inducing a mitochondrion membrane potential drop and cell apoptosis. The carrier-free nanomedicine also has a good blood long-circulation effect and tumor accumulation capability in a body, and an antitumor effect is better than that of a clinical drug, and the carrier-free nanomedicine also has good biological safety. The preparation method is simple, and can be used for preparation of an antitumor drug.

The invention discloses a nano vesicle with tissue targeting and mitochondrial localization as well as preparation and application of the nano vesicle. The nano-vesicle is a nucleus pulposus cell membrane entrapped with a small molecule mitochondrial membrane stabilizer, and tetra-acetylated N-acetamido mannose is added in the culture process of nucleus pulposus cells, so that a sialic acid derivative with an azide group is expressed on the surface of the nucleus pulposus cell membrane. Therefore, triphenylphosphine cations are modified on the surface of the nucleus pulposus cell membrane through a biological orthogonal reaction. The nano-vesicle can stabilize a mitochondrial membrane structure, improve cell aging-related secretion phenotype release and mitochondrial functions, block mtDNA release and SASP factor generation, realize anti-aging, anti-inflammatory and tissue degeneration intervention, can be used for preparing intervention drugs for tissue degeneration diseases related to mitochondrial membrane damage, and has broad application prospects. Or a drug for regulating mtDNA leakage and SASP release in a cell aging model. Wide application prospects and important clinical transformation values are realized.

The present disclosure is directed to compositions comprising mitochondrial optogenetics-based gene therapies and their methods of use. In some embodiments, a composition described herein comprises an expression vector comprising a first nucleic acid sequence encoding a channelrhodopsin fusion protein and a second nucleic acid sequence encoding a luciferase protein. In some cases, the first nucleic acid sequence and the second nucleic acid sequence are operably linked to an expression control sequence. In some instances, the channelrhodopsin fusion protein comprises a channelrhodopsin protein linked to an inner mitochondrial membrane-mitochondrial localization signal (IMM-MLS). In some implementations, when the expression vector is expressed, the luciferase protein is localized to the cytosol. In some cases, the IMM-MLS comprises a leading sequence from a mitochondrial inner membrane protein selected from ABCB10, ABCB140, Cytochrome C, and renal outer medullary potassium channel (ROMK).

The application discloses Bifidobacterium Pseudocatenulatum and application thereof, and the Bifidobacterium Pseudocatenulatum YSBP01CCTCC NO: M 20232067. Experiments prove that the Bifidobacterium Pseudocatenulatum can enhance the antioxidant capacity of Caenorhabditis elegans, prolong the life of the nematode, improve the activity and the reproductive capacity of the nematode, reduce fat accumulation, improve the mitochondrial membrane potential, and delay the aging of the body. The Bifidobacterium Pseudocatenulatum can also significantly inhibit the weight increase of a high-fat-diet mouse, reduce the TG level in serum of the mouse, significantly reduce the fasting blood glucose concentration, and effectively prevent and relieve obesity and type 2 diabetes.

Infarction damage is ameliorated or treated through the administration of a mitochondrial degradation inhibitor, such as one that acts by inhibiting translocation of one or more molecules across a mitochondrial membrane, for example BAX / BNIP3 complexes involved in mitochondrial degradation. By preventing mitochondrial degradation, one allows more efficient oxygenation of an infarcted region, allowing for a greater degree of cell survival and a more successful recovery.

This invention discloses a method for detecting mitochondrial membrane potential in the gills or hepatopancreas of crustaceans, belonging to the field of mitochondrial membrane potential detection technology. This invention, by addressing the structural and physiological differences between gill and hepatopancreas tissues in crustaceans, formulates differentiated incubation strategies: for gill tissue, a "live pre-equilibration-short-time staining-rapid slide preparation" method is used, strictly controlling the JC-1 incubation time to within 10 minutes to effectively avoid probe toxicity damage to mitochondria; for hepatopancreas tissue, in vivo incubation is extended to 1 hour to ensure sufficient dye penetration. Under the condition of uniformly using 2 μM JC-1 and 20 μmol / L CCCP as positive controls, this method significantly improves the tissue penetration and signal uniformity of the dye, solving problems such as uneven staining and weak signal caused by exoskeleton barriers and high lipid content, providing reliable technical support for aquatic health assessment and toxicology research.

The invention discloses a method for synergistically improving the activity of porcine oocytes through low-temperature plasma and erythritol, and belongs to the technical field of reproductive biology. The method comprises the following steps: collecting pig ovaries and separating oocytes; freezing protection is carried out by adopting a freezing liquid (DMSO: EG: FSF = 2: 2: 6) containing 0.5 mol / L erythritol, and preservation is carried out at-80 DEG C for 48 hours; and after unfreezing, treating for 30 seconds by using low-temperature plasma (6.83 kHz, 4.8 kV) to activate the cells. Experiments show that the erythritol can reduce frozen ice crystal damage, and the plasma treatment can significantly improve the cell activity after resuscitation, reduce the ROS content, increase the GSH reserve and enhance the mitochondrial membrane potential. And the survival rate of the oocytes is improved through synergism of the two. The problems that the cell activity is reduced and oxidative damage is serious in the cryopreservation process are solved, and an efficient technical scheme is provided for preservation of pig germplasm resources.

The application discloses a kind of mitochondrial quality control detection methods, the present application relates to mitochondrial quality control detection technical field, operating steps include preparation sample cell suspension, fluorescent dye labeling, cardiomyocyte separation, establish myocardial cell damaged model and detect mitochondrial membrane potential situation.This mitochondrial quality control detection method can simultaneously carry out multi-parameter, rapid quantitative analysis and sorting, measure fast, measure the multi-parameter characteristics of each cell, while carrying out cell characteristic analysis, can separate out the cell of specified characteristics, so as to further culture, cloning, observation or carry out mitochondrial fragmentation test to specific cell, establish myocardial cell damaged model using doxorubicin, the mitochondrial membrane potential situation of normal myocardial cell and damaged myocardial cell obtained by using JC-1 mitochondrial membrane potential fluorescent probe detection is verified the detection quality of this mitochondrial quality control detection method.