166 results about "Microglial cell" patented technology

The invention belongs to the technical field of biological medicine, and particularly relates to an extracellular vesicle drug delivery system, a preparation method thereof and application of the extracellular vesicle drug delivery system in treatment of Alzheimer's disease. According to the invention, one or more of stilbene glucoside, emodin, kaempferol, resveratrol and quercetin are used for regulating and controlling the expression of miRNA (micro Ribonucleic Acid) related to the disease progress in the extracellular vesicles, and the result shows that one or more of miR-let-7c-5p, miR-486-5p, miR-132-3p, miR-160b and miR-129-5p is remarkably up-regulated, and one or more of miR-342-3p, miR-16-5p and miR-125b-5p is remarkably down-regulated. The regulated extracellular vesicles can be used for treating Alzheimer's disease, relieving Tau protein abnormal phosphorylation, reducing amyloid protein beta deposition, inhibiting microglial cell activation, protecting neuronal cells and relieving memory deficits.

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 biomedical engineering, and discloses a biochip screening method of a therapeutic agent based on intestinal brain axis regulation and application thereof. The screening method comprises the following steps: performing intestinal wall cell culture or microglial cell culture by adopting a metasurface plasmon resonance biochip of which the surface is subjected to bionic treatment to obtain an intestinal wall cell adherent chip board or a microglial cell adherent chip board; the method comprises the following steps: adding a culture medium containing a chemotherapeutic drug or lipopolysaccharide into a cell-adherent chip board for culture I, then removing the culture medium, adding a therapeutic agent to be detected for culture II to obtain a culture solution, and detecting the cell repair effect of intestinal wall cells or microglial cells in the culture solution, and screening to obtain a therapeutic agent with a repairing effect on intestinal wall cells and / or microglial cells. The screening method can be used for efficiently and accurately screening the therapeutic agent with dual effects of intestinal regulation and neuroprotection from a plurality of therapeutic agents to be detected, and can be used for dynamically monitoring and exploring the interaction condition of the therapeutic agent and cells on line in an unmarked and real-time manner.

The invention discloses application of eugenin in preparation of a medicine for treating cerebral arterial thrombosis, and belongs to the technical field of medicines. An in-vivo middle cerebral artery occlusion model is adopted, after reperfusion is conducted for 24 h, the cerebral infarction volume and movement coordination function defect of a mouse are detected to evaluate the treatment effect of eugenin, and activation of microglial cells and survival of neuronal cells are observed through immunofluorescence to clarify the action way of eugenin. Pharmacological activity shows that eugenin can obviously reduce the cerebral infarction volume of a model mouse, improve pathological damage of cells and promote recovery of a motion coordination function, and the action way of eugenin is to promote survival of neuronal cells and inhibit activation of microglial cells. Research results indicate that eugenin has the effect of resisting cerebral arterial thrombosis and can be used as a candidate medicine for developing the cerebral arterial thrombosis resisting medicine.

The application relates to the technical field of biological medicine and fundus disease treatment, in particular to application of Acbd3 in treatment of fundus diseases. It is found that the mRNA expression level and the protein expression level of Acbd3 in the retina of a fundus disease model mouse are significantly higher than those of a control group. After an Acbd3 inhibitor is used, the inflammatory reaction and neuron apoptosis in the retina of the fundus disease model mouse are significantly relieved, abnormal activation of Muller cells and microglia cells can be reduced, and a damaged blood-retina barrier can be repaired.

The invention belongs to the technical field of biological medicine, and relates to application of a compound D25, in particular to application of a small molecule compound D25 in preparation of a product for preventing or treating Alzheimer's disease (AD), and the structural formula of the compound is shown in the specification. Experiments prove that the small molecule compound D25 can pass through a blood brain barrier, can induce autophagy, can relieve pathological characteristics of an AD mouse model and improve cognitive impairment of the AD mouse model, can reduce the proportion of disease-related microglial cells by recovering the morphology of the microglial cells and improving the A beta phagocytosis capacity of the microglial cells, has the potential of promoting neuronal growth and increasing the number of protrusions, and can be used for preparing a medicine for treating the disease-related microglial cells. Therefore, AD can be effectively treated, the safety is high, the effect is achieved, and the application prospect is great.

Microglial spatial heterogeneity remains a crucial yet poorly studied question in light of potential cell-directed therapies for Alzheimer`s disease (AD). Little is known about the dynamics of spatially distinct microglia states, which are either adjacent or non-associated with the plaque site, and their selective contributions to neurodegeneration in vivo. So far, research has essentially focused on pathology-associated microglia. Here, we combined novel multicolor fluorescence fate mapping, single-cell transcriptional analysis, epigenetic profiling, advanced immunohistochemistry and computational modelling to comprehensively characterize the relation of plaque-associated and non-plaque- associated microglia during neurodegeneration. This approach enabled us to identify and characterize non-plaque-associated microglia as a unique and highly dynamic microglial state in a mouse model of AD. Non-plaque-associated microglia modulate network expansion, quickly adapt to environmental cues and their transition to plaque-associated microglia can be specifically modulated during disease, contrary to their reputation as a passive bystander subpopulation. This description of the dynamics of spatially segregated microglial states and their distinct molecular features may therefore open promising new avenues for state-specific therapeutic interventions during neurodegeneration.

This invention relates to diselenylene-bridged mesoporous silica nanoparticles loaded with baicalin and their applications. The invention constructs a ROS-responsive, microglia-inspired Ba@Se-MSN&BV2 nanoplatform targeting the secondary phase of spinal cord injury. The BV2 cell membrane-mediated enrichment at the injury site, combined with the diselenylene-triggered, on-demand release of baicalin, enables targeted intervention in a highly oxidative and pro-inflammatory microenvironment. In vitro and in vivo studies show that Ba@Se-MSN&BV2 can alleviate oxidative stress and mitochondrial dysfunction, inhibit apoptosis, promote axonal and neuronal survival, and improve motor circuit function. This invention provides a new therapeutic target and research direction for neuroinflammatory injuries driven by redox homeostasis disruption, with significant clinical application prospects and social value.

The application discloses a new use of Leonurine or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating radiation-induced brain injury, specifically, providing a safe and effective therapeutic drug for iron death, neuroinflammation, neuron damage and lipid metabolism disorder accompanying the radiation-induced brain injury, solving the technical problem of lack of specific treatment means in the prior art, and having a wide clinical application prospect. Experiments adopt a C57BL / c mouse 30 Gy whole brain X-ray radiation model, and results show that Leonurine can significantly improve the body weight decrease and survival rate of the model mice, reduce the serum IL-6 and IFN-alpha levels, inhibit the activation of microglial cells in the cerebral cortex and hippocampus, protect and repair damaged neurons, and improve the ultrastructure of mitochondria and synapses; meanwhile, the expression of GPX4 and SLC7A11 proteins in the brain tissue is up-regulated, the GSH content is increased to inhibit iron death, and the levels of GPE, GPS and GPC related to lipid metabolism are restored.

The invention discloses an application of abscisic acid in preparation of a medicine for improving secondary brain injury after cerebral hemorrhage, the abscisic acid can relieve neuroinflammation and improve neurological function recovery by repairing microglial cell lysosome functions, enhancing phagocytic ability and promoting hematoma removal, and a new medicine strategy is provided for cerebral hemorrhage treatment.

The invention discloses an application of a pyruvate dehydrogenase kinase (PDKS) inhibitor in preparation of a composition for treating Alzheimer's disease (AD), and particularly discloses an application of the PDKs inhibitor in preparation of the composition for treating the AD. According to the invention, the level of oxidative phosphorylation (OXPHOS) of microglial cells is obviously enhanced, the inflammatory response of the microglial cells is effectively reduced, the migration and aggregation capabilities of the microglial cells are obviously improved, the capability of the microglial cells to phagocytize and degrade extracellular beta-amyloid protein (A beta) plaque is obviously enhanced, the cognitive function defect of AD model mice is effectively improved, and the application of the microglial cells in the treatment of the AD model mice is promoted. The preparation is simple, and the application is wide.

The present invention provides methods and compositions for the generation of microglial progenitor cells and microglial cells from pluripotent stem cells, such as embryonic stem cells and induced pluripotent stem cells. The present invention also provides cells produced using such methods, and both methods of treatment and methods of drug screening that use such cells. Also provided are various tissue culture media, tissue culture media supplements, and kits useful for the generation of human microglial progenitor cells and human microglial cells.

The invention discloses an mGluR5 small-molecule allosteric modulator and application thereof in inhibition of neuroinflammation, and belongs to the technical field of neuropharmacology and anti-inflammatory drug research, two mGluR5 small-molecule allosteric modulators are obtained by virtual screening through an allosteric pocket targeting mGluR5, the structural formulas of the two mGluR5 small-molecule allosteric modulators are shown in the specification, and the structural formula of the mGluR5 small-molecule allosteric modulators is shown in the specification. The mGluR5 micromolecule allosteric modulator can be used for inhibiting microglial cell inflammation, and can effectively relieve LPS-induced microglial cell NO release.

The application provides application of dimethyl itaconate in prevention and treatment of chronic stress-induced anxiety. The application finds that dimethyl itaconate can inhibit excessive activation of microglial cells in a stress state, improve mitochondrial structure and function abnormalities of the microglial cells, and reduce expression of a lysosome marker CD68, so as to inhibit central nervous inflammation, maintain central nervous immune homeostasis, prevent and relieve anxiety-like behavior induced by chronic stress, and effectively prevent and relieve occurrence and development of chronic stress-induced anxiety (generalized anxiety disorder).

The present application relates to a kind of microglial cell P2Y6R target point inhibitor and its application, belong to biological medicine technical field.For the problems such as lack of effective treatment means for retinal pigment degeneration, abnormal activation of microglial cell accelerates course and lack of specific intervention target point, the application of inhibitor with P2Y6R as target point in preparation treatment retinal pigment degeneration drug is proposed, especially siRNA and shRNA for knocking down microglial cell P2ry6 gene are provided, and AAV vector containing microglial cell specific promoter is constructed, the specific silencing of P2ry6 in retina is realized.The present application can significantly inhibit abnormal activation of microglial cell and inflammatory response, reduce photoreceptor apoptosis, improve retina structure and visual function, and provide a new strategy for targeted treatment of retinal pigment degeneration.

The invention relates to the technical field of biological medicine, and particularly discloses a macrophage membrane coated plateau encephaledema drug carrier and a preparation method and application thereof, and the macrophage membrane coated plateau encephaledema drug carrier is composed of a nanoparticle core and a macrophage membrane shell layer wrapping the core; the nanoparticle core comprises an ROS-responsive carrier material and carbon monoxide release molecules MnCO entrapped in the ROS-responsive carrier material; the content of phosphatidylserine in the shell layer of the macrophage membrane is not less than 5 mol% of the total phospholipid of the membrane. According to the invention, a bionic delivery system of ROS response type MnCO nanoparticles coated with a macrophage membrane is constructed, phosphatidylserine on the surface of the membrane is utilized to actively activate a microglial cell Trem2 receptor, a positive feedback cycle of targeting phagocytosis-CO release-Trem2 up-regulation is formed, and at the same time, fatty acid oxidative metabolism reprogramming is promoted by means of degraded membrane lipid, so that the biomimetic delivery system is used for preparing the ROS response type MnCO nanoparticles. And multi-mechanism synergistic efficient brain-targeted therapy is realized.

This invention relates to the application of LAG3 agonists in the preparation of drugs for hematoma clearance after intracerebral hemorrhage (ICH) and the application of LAG3 in regulating hematoma clearance after ICH, belonging to the field of biomedical technology. This invention utilizes a mouse ICH model to first inject a LAG3 neutralizing antibody (C9B7W) via orthotopic injection, clarifying that LAG3 can regulate the phagocytic function of microglia after ICH and participate in hematoma clearance, revealing its potential molecular target for enhancing microglia phagocytic function and promoting hematoma clearance. Furthermore, overexpression of LAG3 after ICH is demonstrated. Lag3 The study confirmed that enhanced phagocytic function of microglia accelerated hematoma clearance, demonstrating that LAG3 agonists can be used as drugs for hematoma clearance after intracerebral hemorrhage. The experimental results of this invention make it possible to apply LAG3 to the prognostic treatment of ICH, thereby advancing basic and clinical research on endogenous hematoma clearance after ICH.

The invention belongs to the technical field of medicines, and relates to injectable piezoelectric hydrogel for a spinal cord injury part as well as a preparation method and application of the injectable piezoelectric hydrogel. According to the hydrogel, methacrylated gelatin is used as a carrier, and a piezoelectric material MOF (at) PDA (at) M0, namely MP (at) M, of an enveloping porous structure is loaded in the hydrogel. The hydrogel can achieve dual functions under the ultrasonic action: (1) MP (at) M has piezoelectricity, ultrasonic mechanical energy is converted into electrical stimulation, calcium ion inward flow of astrocytes is triggered, mitochondria is promoted to be transferred from the astrocytes to neurons, and the mitochondrial function of the neurons is recovered; (2) the CD73 enzyme carried by the microglial cell membrane coated on the surface of the MP (at) M can degrade pro-inflammatory ATP (adenosine triphosphate) at the damaged part to generate adenosine, so that astrocytes are promoted to release lactic acid, and rapid energy support is provided for neurons. Mitochondrial transfer and energy supply are synchronously promoted through ultrasonic stimulation, neuronal plasticity is remodeled, spinal cord axon regeneration is promoted, and a new strategy is provided for spinal cord injury treatment.

This invention provides the application of fractalkine in the preparation of drugs for the prevention or treatment of white matter injury repair. In animal models of cerebral hemorrhage, it was found that the mass effect of hematoma in the basal ganglia and the neurotoxic products generated by its lysis lead to damage to surrounding white matter fiber bundles. Fractalkine plays an important role in regulating microglial activation after cerebral hemorrhage to promote white matter repair.

The invention belongs to the technical field of medicines, and discloses application of a compound M1 shown as a formula (I) and pharmacodynamically acceptable salt thereof in preparation of medicines for preventing, relieving and / or treating autoimmune demyelination diseases. On a mouse experimental autoimmune encephalomyelitis model, the compound M1 shows a good treatment effect, can effectively prevent and treat pathological changes and disease progression of diseases, relieve the severity of the diseases and inhibit LPS-stimulated microglial BV2 cells from releasing inflammatory mediators, and provides a new drug and a new structure for clinical treatment.

The invention provides a cassane diterpenoid compound and an application of the cassane diterpenoid compound in preparation of an anti-neuroinflammation medicine. Six novel cassane diterpenoid compounds are separated from mysorethorn, and a preparation method of the six compounds is provided. According to the present invention, the inhibition effect of lipopolysaccharide (LPS)-induced BV-2 microglial cells on NO production is determined, and the six compounds have anti-neuroinflammatory activity, and particularly, the compounds 4 and 5 have good anti-inflammatory effect compared with other compounds, and have the potential of anti-neuroinflammatory drug preparation.

The present invention provides use of lifitegrast in the preparation of a drug for treating retinal artery occlusion injury. Lifitegrast can effectively reduce retinal artery occlusion injury and apoptosis of retinal ganglion cells and has the effect of inhibiting inflammatory infiltration in the retina and activation of microglia. Moreover, lifitegrast has the effect of reducing retinal ganglion cell injury. Lifitegrast can be used for related diseases such as neuroinflammatory injury caused by retinal artery occlusion.

This invention discloses a micropeptide, its encoding nucleic acid, and its application in regulating inflammatory activation of microglia. The amino acid sequence of the micropeptide is shown in SEQ ID NO:3. Simultaneously, this invention discloses the nucleic acid encoding the micropeptide, which contains either the nucleotide sequence shown in SEQ ID NO:1 or the nucleotide sequence shown in SEQ ID NO:2, wherein SEQ ID NO:2 is a small open reading frame located within the sequence of SEQ ID NO:1. This invention validated the translational expression of the micropeptide in microglia by constructing an EGFP reporter gene fusion vector and a SUMO tag fusion expression vector. Functional experiments showed that under oxygen-glucose deprivation / reperfusion injury conditions, the micropeptide significantly inhibited inflammatory activation of microglia. This invention provides a new potential target and candidate drug for the treatment of neuroinflammatory diseases such as stroke.

The present invention relates to the provision of novel sources of microglia-like cells having a unique phenotype. In particular, the present invention relates to medical uses of such microglia-like cells, in particular in relation to treatment of neurodegenerative diseases.

The invention belongs to the technical field of biology, and particularly relates to a construction method of a respiratory syncytial virus infected mouse model. Disodium clodronate liposome with the concentration of 4ng / mL is injected into the lateral ventricle of the mouse through stereotactic positioning of the brain. 48h after injection, mouse brain tissues are taken to detect the activation state of microglial cells through immunofluorescence and WB, after it is confirmed that the microglial cells are inhibited, RSV (virus titer: 2.8 * 10 < 6 > PFU) nasal drop infection experiments are carried out on the mouse, and after the 5th day after virus infection, the mouse is infected by the RSV (virus titer: 2.8 * 10 < 6 > PFU) nasal drop infection experiments. Likewise, mouse brain tissue is taken for virus load detection, and neuropathological changes of the mouse brain tissue are observed through HE staining, immunofluorescence and TUNEL staining, so that the method can be used for constructing a research model of RSV-related nervous system diseases.

The present application relates to a Pediococcus acidilactici capable of reducing the activation of hippocampal microglia cells and its application, belonging to the technical field of microorganisms. The Pediococcus acidilactici described in the present application is Pediococcus acidilactici CCFM1344, which was preserved in the Guangdong Microbial Culture Collection Center on September 12, 2023, with the preservation number GDMCC NO.63800. The preservation address is Building 59, 5th Floor, Guangdong Microbial Institute, 100 Middle Martyrs Road, Guangzhou. The Pediococcus acidilactici described in the present application can inhibit the over-activation of microglia cells caused by chronic stress, reduce the concentration of pro-inflammatory factors in the hippocampus of the brain, thereby relieving the activation of microglia cells in the hippocampus of the brain caused by chronic stress, and has excellent application prospects.

To provide compounds and compositions for reducing most common opioid-induced hyperalgesia associated with microglial hyperactivation.SOLUTION: 2-pentadecyl-2-oxazoline (PEA-OXA) for use as an opioid adjuvant for preventing the development of or in the treatment of opioid-induced hyperalgesia (OIH), wherein the PEA-OXA is administered with or in combination with an opioid. Wherein the administration is separate, together or simultaneous.SELECTED DRAWING: None

A branched chain fatty acid composition, and a use thereof in regulating brain nerve immunity. The branched chain fatty acid composition comprises C15:0 and C17:0. By using the branched chain fatty acid composition to promote LPS-induced microglia, the tendency to promote the differentiation of microglia into M2-phenotype microglia is higher than the tendency to promote the differentiation of microglia into M1-phenotype microglia. Also, the secretion of anti-inflammatory factors such as IL-4 and IL-10 is promoted, and the secretion of pro-inflammatory factors such as NO, TNF-a and IL-1β is inhibited. C15:0 and C17:0 in the branched chain fatty acid composition have a good synergistic effect, and have the function of regulating brain nerve immunity.

The application discloses a kind of bioengineered apoptotic bodies based on apoptotic body membrane protein and liposome and preparation method and application thereof.The bioengineered apoptotic bodies are formed by the chimerization of apoptotic body membrane protein and liposome loaded with gastrodin and Cy5.The bioengineered apoptotic bodies simulating the natural apoptosis process of mesenchymal stem cells can promote the polarization of microglial cells to M2 type, release anti-inflammatory factors and neurotrophic factors, promote the proliferation of neurons, improve the antioxidant capacity of cells, improve the nervous motor function, relieve brain edema, and thus effectively treat traumatic brain injury.

The application discloses a medicine composition for inhibiting inflammatory activation of microglial cells and application thereof. 6-gingerol and eucommia alcohol are combined with each other, and the combination has a significant synergistic effect, and can effectively inhibit inflammatory activation of microglial cells.