229 results about "Microglial cell" patented technology

The invention which relates to the medicinal field discloses an application of butylphthalide and derivatives thereof in the preparation of medicines for preventing and treating ALS (amyotrophic lateral sclerosis). Butylphthalide and the derivatives, which can delay the disease time of an SOD1-G93A transgenic mouse, prolong the lifetime of the mouse, reduce the degenerative change of spinal motorneurons, obviously increase the survival number of spinal anterior horn motor neurons of the mouse, reduce the electrophysiological abnormality of the transgenic mouse, obviously improve the action potential amplitude and the motion unit number of compound muscles, substantially inhibit the activation of astrocytes and microglial cells in the spinal cord of the mouse, and obviously reduce the expression level of iNOS and NF-kappaBp65, have good application prospects in the prevention and the treatment of the ALS.

Disclosed is a therapeutic method comprising administering a TIM-3 antibody to a subject who is suspected to be suffering from blood tumor and in whom TIM-3 has been expressed in a Lin(−)CD34(+)CD38(−) cell fraction of bone marrow or peripheral blood or a subject who has been received any treatment for blood tumor. Also disclosed is a composition for preventing or treating blood tumor, which comprises a TIM-3 antibody as an active ingredient. Conceived diseases include those diseases which can be treated through the binding or targeting of the TIM-3 antibody to blood tumor cells (AML cells, CML cells, MDS cells, ALL cells, CLL cells, multiple myeloma cells, etc.), helper T cell (e.g., Th1 cells, Th17 cells), and antigen-presenting cells (e.g., dendritic cells, monocytes, macrophages, and cells resembling to the aforementioned cells (hepatic stellate cells, osteoclasts, microglial cells, intraepidermal macrophages, dust cells (alveolar macrophages), etc)), all of which are capable of expressing TIM-3. The diseases for which the therapeutic use is to be examined include blood diseases in which the expression of TIM-3 is observed in bone marrow or peripheral blood, particularly blood tumor.

Disclosed are methods and compositions for delivering a therapeutic agent to target organs or tissues, such as brain. The methods and compositions use bone marrow stem cells, monocytes, macrophages or microglial cells to deliver the therapeutic agent associated with nanoparticles to the target organ or tissue.

The invention provides a compound. The compound and pharmaceutically acceptable salt, various isotopes, various crystal forms or various isomers have the structure shown as a formula (I): A-L-B (I), wherein A is a non-steroidal anti-inflammatory drug compound monomer, B is a hydrogen sulfide releaser or an antioxidant compound, and L is a group or a functional group which connects A and B. The invention further provides an application of the compound as a medicine for inhibiting neuroinflammation as well as a combined application of the compound and other drugs as medicines for inhibiting neuroinflammation. By applying the concept of double prodrugs, the non-steroidal anti-inflammatory drug and the hydrogen sulfide releaser or the antioxidant compound are covalently connected together to form a multiple-target point compound which can effectively inhibit inflammatory response of the microglial cell induced by lipopolysaccharide, so that the compound can be used for treating or preventing various neurodegenerative diseases.

The invention discloses an application of gastrodin to preparing medicaments for preventing and treating Alzheimer's disease. Alzheimer's disease (AD) is a neurodegenerative disease, and pathological characteristics comprise neuro fibrillary tangles formed in cells, hyperplasia of reactive microglia and glial cell, and the like, wherein the extracellular deposition of amyloid A beta is the main pathogenetic reason of AD. An AD small mouse taking a gastrodin-containing fodder is substantially improved in spatial-memory learning ability, substantially reduced in A beta level in brain and serum, and substantially reduced in amyloid plaques and microglia in brain tissue, and thus it is indicated that gastrodin is capable of preventing A beta deposition and decreasing active components causing AD mouse brain gastrodin.

The invention provides application of a P2Y4 receptor stimulant in preparing medicaments for treating the Alzheimer's disease. The application of the P2Y4 receptor stimulant in preparing medicaments for treating the Alzheimer's disease has the beneficial effects that the P2Y4 receptor stimulant can be used for effectively promoting the pinocytosis to beta-amyloid polypeptide of microglial cells so as to relieve and even cure the Alzheimer's disease; and the P2Y4 receptor stimulant has lower toxicity and low risk and is clinically applied to treating various diseases, thus the P2Y4 receptor stimulant has good application prospect in treating the Alzheimer's disease.

The invention discloses application of a polypeptide for preparing medicine for treating the Alzheimer disease. The amino acid sequence is shown in SEQ ID NO:1. The polypeptide is an extracellular section 41-81 amino acids of a TREM2 receptor protein, and the nucleotide sequence is shown in SEQ ID NO:2. The polypeptide has the application that the microglial mediated inflammation reaction is promoted, apoptosis of microglial cells is restrained, the migration capability of microglial cells is enhanced, Abeta endocytosis and degradation of the microglial cells are promoted, the density of microglial cells inside a brain is increased, and Abeta amyloid plaque deposition inside the brain is lowered.

The invention relates to application of genipin in prevention or treatment of ischemic brain injury. Brain injury is particularly related to injury of microglial cells or human umbilical vein endothelial cells. The invention further relates to a medicine composition containing genipin for preventing or treating ischemic brain injury.

The invention belongs to the technical field of medical instruments, and specifically relates to a phototherapy device for cervical spondylosis. The phototherapy device of the invention comprises a light illumination module, a light path adjustment module, a power supply module and a light adjustment module. The light illumination module is composed of a flexible circuit substrate and a light source for illuminating target cells. The light path adjustment module diffuses light emitted by the light source and distributes the light in a light illumination area uniformly. The light adjustment module is used to set pulse light wavelength, pulse light power and illumination time. Compared with existing therapeutic apparatuses, the phototherapy device of the present invention realizes higher-intensity illumination and has higher penetration depth in tissues. The phototherapy device of the present invention enhances activity of macrophages through an appropriate light mode, accelerates removal of necrotic debris of tissues and cells at lesions of a body while enhancing activity of microglial cells and promoting repair of the central nervous system. In addition, the phototherapy device ofthe present invention uses pulse width modulation to generate pulse light with an extremely strong transient power, thereby avoiding the problems such as small illumination area and reduced penetration depth of laser light in the tissues in infrared-type therapeutic instruments.

The invention relates to the field of biotechnology, and in particular to application of dental pulp mesenchymal stem cells in treatment of Alzheimer disease. According to the invention, through experimental research, it is found for the first time that transplantation of dental pulp mesenchymal stem cells can inhibit chronic inflammation of the brain, improve learning and memory capacity and movement capacity to a certain extent, reduce number of microglia in each region of the hippocampus, and effectively treat Alzheimer disease.

The present invention provides compositions and methods for the treatment or prevention of a neurological disease or disorder of the central nervous system (e.g., a storage disorder, lysosomal storage disorder, neurodegenerative disease, etc.) by reconstitution of brain myeloid cell and microglia upon transplantation of hematopoietic cells enriched in microglia reconstitution potential. The invention also provides compositions and methods for ablating and reconstituting microglia.

The invention discloses a zebra fish brain trauma model and a preparation method and application thereof. The preparation method of the zebra fish brain trauma model includes the steps that for an embryo in the 3dpf period, a needle is used for puncturing the hindbrain of a zebra fish, and microglial cells of the hindbrain of the zebra fish are labeled with fluorescent protein. After clinical first-line anti-inflammatory drugs are used for intervention, and more microglial cells can be activated to migrate and aggregate towards a wound part, so that injured hindbrain repairing is promoted; themicroglial-cell transgenic zebra fish brain trauma model can be used for rapid screening of drugs, so that an economical, convenient and reliable research model is provided for enterprise drug research and development and for evaluating the curative effect of the anti-inflammatory drugs in clinical brain trauma, encephalitis and other diseases, and the microglial-cell transgenic zebra fish braintrauma model has good application prospects and high application value.

The invention relates to a nano-drug for preventing or treating cerebral ischemia-reperfusion injury as well as a preparation method and application of the nano-drug. Cerebral ischemia is a cerebrovascular disease which has the greatest threat to human beings, and oxidative injury, inflammatory response and subsequent excitotoxic cell death can be caused by reperfusion as soon as possible. According to the nano-drug, dopamine is oxidized under an alkaline condition to form dopamine quinone, the dopamine quinone is further oxidized to form polydopamine nanoparticles with supramolecular structures, the formed particles are smooth and round in surface, good in sphericity degree and uniform in particle size distribution, a good dispersion state is kept in a solution, and through in-vitro and in-vivo experiments, the polydopamine nanoparticles prove the biological safety. Application of the polydopamine nanoparticles to a cerebral ischemia model shows that the polydopamine nanoparticles canrelieve cerebral ischemia-reperfusion injury, inhibit inflammatory reaction, inhibit activation of an NF-kappa B signal channel and inhibit excessive activation of microglial cells, and have the potential of inhibiting cerebral inflammatory reaction and relieving cerebral ischemia-reperfusion injury.

The invention aims to provide application of an inhibitor SB (Sodium Butyrate) 203580 of p (phosphor)-p38. Activation of phosphor-p38 mediated microglial cells contributes to pain correlated responses of a pain model of BmKI (Biomedical Knowledge Integration); the specific inhibitor SB 203580 of the p-p38 can inhibit the microglial cell and thus relieving the pain correlated responses in the pain model of the BmKI. The invention provides a theoretical basis for pain central sensitization induced by peripheral damages, a study carrier for studying cellular and molecular mechanisms and treatment strategies of nociception and an experimental basis for studying novel drugs for relieving the pain on clinic are provided. The SB 203580 has a prospect of becoming a tool medicine applied in studying correlated pain mechanism of p38 signal path and then has a potential prospect of developing drugs for treating and relieving pathological pain and maintaining corresponding drugs on clinic.

The invention discloses application of saikoside compounds in preparation of drug for treating neurodegenerative diseases. Five saikoside compounds are saikoside a, saikoside b1, saikoside b2, saikoside c and saikoside d which can remarkably inhibit release of LPS-induced microglial cell inflammation factors NO and ROS, and saikoside a can obviously shorten escape latency and escape distance of mice with LPS-induced learning memory impairment; in a nesting experiment, saikoside a can obviously enhance nesting ability of the mice with the LPS-induced mice with learning memory impairment. The above results show that saikoside a has obvious protecting effect on LPS-induced AD mouse learning memory impairment. Consequently, saikoside a, b1, b2, c and d can be used for treating the neurodegenerative diseases and inhibiting neuroinflammation.

The invention provides an application of extracellular vesicles derived from mesenchymal stem cells in treatment of subarachnoid hemorrhage, which belongs to the technical field of molecular biology.The MSCs extracellular vesicles (MSCs-EVs) have the effects of relieving SAH complications, and improving prognosis and the like. Specifically, the MSCs-EVs can effectively improve the neuroinflammation reaction after subarachnoid hemorrhage (SAH), promote the phenotypic transformation of microglial cells to M2, and relieve the symptoms of neurological impairment, cerebral water content increase and the like caused by subarachnoid hemorrhage.