50 results about "Neuronal damage" patented technology

The invention relates to the technical field of related drugs for nerve injury caused by heavy metal pollution, in particular to application of a compound for inhibiting phosphorylation of ARMC10 in preparation of drugs for antagonizing tin-induced nervous system injury. Exposure of trimethyltin chloride induces nerve cell mitochondrial dysfunction, and the key mechanism is ARMC10 serine 43 site abnormal phosphorylation. Phosphorylated protein causes excessive mitochondrial fission, membrane potential collapse and energy metabolism disorder, resulting in neuron damage. Based on the target spot, a compound for antagonizing tin-induced nervous system injury is obtained through screening, protein phosphorylation can be specifically inhibited, mitochondrial dynamic unbalance and dysfunction induced by trimethyltin chloride are effectively reversed, and neurotoxicity is relieved. According to the technical scheme, the technical problem that in the prior art, no medicine for effectively antagonizing tin-induced nervous system injury exists can be solved, and the compound has the application potential for treating the nervous system injury and cognitive impairment caused by tin exposure.

The invention discloses application of ginsenoside Rg5 in preparation of a medicine for treating Alzheimer's disease and an evaluation method, and relates to application of ginsenoside Rg5 in preparation of a medicine for treating Alzheimer's disease. The medicine improves A beta deposition, tau protein phosphorylation and neuron damage by adjusting the intestinal flora structure and metabolite level, and is used for relieving the pathological process of the Alzheimer's disease. The invention has the characteristics of multi-target effect, nerve protection, inflammation resistance and oxidation resistance.

The invention discloses application of a miR-5588-3p inhibitor, and belongs to the technical field of biological medicines. Researches find that the expression of miR-5588-3p in the plasma of an epileptic is abnormally increased. The miR-5588-3p inhibitor is given 72 hours before the tree shrew epilepsy model is constructed, so that the attack level, the convulsion rate and the death rate of the epilepsy tree shrew can be effectively reduced, and the brain pathological injury of the epilepsy tree shrew can be relieved. The miR-5588-3p inhibitor disclosed by the invention is used for preparing a medicine for treating epilepsy, and the nucleotide sequence of the miR-5588-3p inhibitor is as follows: GCUGGCAUUAGUGGGACUU. According to the present invention, the convulsion rate and the death rate of the epilepsy tree shrew can be well reduced, the matrix incubation period and the convulsion incubation period of the epilepsy tree shrew can be effectively prolonged, the convulsion duration of the epilepsy tree shrew can be shortened, the attack level of the epilepsy tree shrew can be effectively reduced, and the miR-5588-3p inhibitor can significantly reduce the hippocampal neuron damage.

Antibodies that specifically bind to TrkB and methods for using the same are described. Neuroprotective agonist antibodies are described, as indicated by their effect on enhancing the survival of retinal ganglion cells in vitro, and these agonist antibodies may be used to treat eye disorders, such as glaucoma. Additionally, other neuronal diseases or disorders, including those characterized by partial neuronal damage, benefit from treatment using these agonist antibodies. In certain embodiments, the present invention comprises antibodies that bind to TrkB and mediate cell signaling. The antibodies of the present invention may be whole human, non-natural antibodies formulated as injectable excipients.

The invention discloses application of Cacumen biotae-derived extracellular vesicles in preparation of drugs for treating anxiety, depression or insomnia. The EVs are separated and purified from cacumen biotae through a specific differential ultracentrifugation method, the EVs have a typical double-layer membrane structure, the average particle size is about 100 nm, about 1012 EVs can be extracted from each gram of cacumen biotae, and 62 volatile components are contained. Cacumen biotae EVs can be taken by PC12 cells, and corticosterone-induced neuron damage can be relieved; for chronic constraint stress model mice, anxiety behaviors and spatial learning and memory disorders can be improved, and central nervous inflammation can be inhibited; for chronic unpredictable mild stress model mice, the weight, the sucrose preference rate and the cognitive ability can be recovered, and the levels of 5-hydroxytryptamine and gamma-aminobutyric acid are increased; and for 4-chloro-DL-phenylalanine induced insomnia model mice, the sleep condition can be improved, the neurotransmitter level can be recovered, and the effect is equivalent to that of positive drugs such as citalopram, fluoxetine, diazepam and the like.

The invention discloses a resveratrol-loaded Prussian blue / tetrahedral framework nucleic acid nanocomposite and application thereof in preparation of a medicine for treating epilepsy. The nano-composite (R-tFNAs (at) PB) takes Prussian blue (PB) nano-enzyme as a core, and tetrahedral framework nucleic acid (tFNAs) loaded with resveratrol (Res) is anchored on the surface of the nano-composite (R-tFNAs (at) PB). The nanocomposite has excellent blood-brain barrier (BBB) penetrating ability and focus targeting ability, and can specifically gather in epilepsy hippocampus focus. In mechanism, the compound enhances the oxidation resistance of mitochondria by synergistically removing reactive oxygen species (ROS) and activating an SIRT3 / SOD2 signal channel, further inhibits activation of NLRP3 inflammasomes, and promotes polarization of microglial cells from a pro-inflammatory M1 type to an anti-inflammatory M2 type. In-vivo and in-vitro experiments show that the compound can significantly reduce neuron damage, reduce epileptic seizure frequency and severity, and significantly improve cognitive impairment caused by epilepsy, and has good biological safety.

Antibodies that specifically bind to TrkB and methods of use thereof are disclosed. Agonist antibodies having neuroprotective effects, as shown by their ability to enhance retinal ganglion cell survival in vitro, are disclosed, and these agonist antibodies can be used in the treatment of conditions such as eye diseases, including glaucoma. In addition, other neuronal diseases or conditions can also benefit from treatment with these agonist antibodies, including those characterized in part by neuronal damage. In certain embodiments, the present invention includes antibodies that bind to TrkB and mediate cell signaling. The antibodies of the present invention can be fully human, non-naturally occurring antibodies formulated with an excipient for injection.

The invention relates to the technical field of preparation and application of traditional Chinese medicine compositions, and particularly discloses a traditional Chinese medicine composition for treating Alzheimer's disease and a preparation method and application thereof. The traditional Chinese medicine composition is prepared from the following traditional Chinese medicine raw materials in parts by weight: 9-30 parts of astragalus membranaceus, 9-30 parts of codonopsis pilosula, 6-10 parts of herba epimedii, 9-15 parts of rhizoma polygonati, 3-10 parts of rhizoma acori graminei, 3-10 parts of polygala tenuifolia, 6-12 parts of dendrobe, 3-6 parts of rhodiola rosea, 3-10 parts of radix curcumae, 9-15 parts of cortex lycii radicis, 3-9 parts of Hubei fritillary bulb, 3-10 parts of radix angelicae, 3-10 parts of pericarpium citri reticulatae and 3-10 parts of fresh ginger. The traditional Chinese medicine composition provided by the invention accords with the traditional Chinese medicine treatment concept of tonifying deficiency and filling marrow, inducing resuscitation and soothing nerves, dredging collaterals and eliminating evil, and tonifying spleen and assisting transportation, not only can relieve damage of neurons, but also can reverse alzheimer disease related disorder signal channels in neuronal cells, microglial cells and astrocytes.

The inventions relates to Immunoglobulin A (IgA) or a pharmaceutical composition comprising IgA for use in the treatment of an infectious disease of or in an immune privileged organ, such as the eye, fetus, placenta, central nervous system (CNS) and / or testicles caused by a bacterial, fungal, viral or parasitic infection, in particular caused by bacteria of the human microbiome. IgA-coated pathogens can be addressed by FCAR+ and / or CD11c+ innate immune cells, for example by phagocytosis, or by activation of the complement system. The use of IgA or a pharmaceutical composition comprising IgA in immune privileged sites is advantageous because in contrast to IgG, IgA-coated pathogens do not trigger activation of C1q, a protein used for the controlled pruning of synapses. This prevents neuronal damage in said immune privileged organ(s), while at the same time allowing an antibody-mediated immune response in said organs.

The present invention relates to a cerium oxide nanocomposite, a method for preparing the same, and a composition for preventing or treating inflammatory or autoimmune diseases comprising the cerium oxide nanocomposite as an active ingredient. The present invention can be used as an excellent therapeutic composition in which the surface of cerium oxide nanoparticles is modified with an optimal content of a pyrrolidone-derived polymer to maximize both biological stability and in vivo reactive oxygen scavenging efficiency at the same time. Furthermore, the nanocomposite preparation method of the present invention can prepare uniform particles having an optimal diameter while thoroughly removing reaction residues and nitrate-derived toxicity by a simple process in which washing is performed using a sodium chloride solution of a specified concentration. The nano-composite disclosed by the invention can be used for remarkably inhibiting inflammatory reactions in various tissues. The composition is especially suitable for being used as an excellent treatment composition, and neuronal damage caused by excessive inflammatory reaction in hematoma surrounding areas after cerebral hemorrhage can be reduced to the maximum extent, so that the neurological function is recovered, and the survival rate of patients is remarkably increased.

The present invention relates to a novel association or combination of active ingredients useful in the prevention and repair of neuronal damage, both centrally and peripherally. In greater detail, the present invention relates to an association or combination of an extract of Gastrodia elata, citicoline, L-acetylcamitine, at least one vitamin of group B and at least one vitamin of group D. Furthermore, the invention also relates to the pharmaceutical compositions and / or compositions for medical devices and / or nutraceutical and / or food compositions comprising that association and to their use in therapy, in particular in the protection of the functionality of the central and of the peripheral nervous system.

The invention relates to the technical field of biological medicine, and particularly discloses application of a cGAS-STING pathway inhibitor in relieving neural immune response induced by AAV, and the technical key points are as follows: it is found that high-dose AAV can activate a cGAS-STING signal pathway in a nervous system, resulting in inflammatory response, glial cell activation, T cell infiltration and neuron damage; the cGAS-STING pathway is inhibited by means of gene knockout (Stin < + / ->), pharmacological inhibition (such as STING inhibitor H-151) or virus-mediated gene knockout (shSTING) and the like, so that the AAV-induced immune response and neurotoxicity can be effectively reduced, and meanwhile, the expression of a transgenic product carried by the AAV vector is improved. The scheme provided by the invention provides a new strategy and means for optimizing the safety-effectiveness balance of AAV gene therapy.

The invention discloses application of an amide compound in preparation of a medicine for treating Alzheimer's disease, and belongs to the technical field of medicines, and the amide compound is N-[(1S)-1-(furan-2-yl) ethyl]-6-nitro-2, 3-dihydro-1, 4-benzodioxin-7-formamide. According to the application of the amide compound in preparation of the medicine for treating the Alzheimer's disease, N-[(1S)-1-(furan-2-yl) ethyl]-6-nitro-2, 3-dihydro-1, 4-benzodioxin-7-formamide can be used for preparing the medicine for treating the Alzheimer's disease by regulating cholinergic system functional defects and inhibiting oxidative stress neuron damage, so that the Alzheimer's disease can be effectively treated. Multi-target accurate intervention on diseases is achieved, the treatment effect is improved through the synergistic effect, and a new thought is provided for treatment of the Alzheimer's disease.

The invention discloses application of lncRNA-DCST1-AS1 in preparation of a medicine for treating cerebral arterial thrombosis, and relates to the technical field of biomedicine. The invention finds that after expression of lncRNA-DCST1-AS1 is up-regulated, the activity of neurons subjected to hypoglycemia and hypoxia reperfusion can be further inhibited, and neuronal injury and apoptosis are promoted. By down-regulating and intervening the lncRNA-DCST1-AS1, the occurrence of cerebral ischemia / reperfusion injury can be avoided, and the lncRNA-DCST1-AS1 has an obvious protection effect on neuronal injury caused by sugar deficiency and hypoxia reperfusion, can obviously improve the cell activity and reduce the cell apoptosis caused by the neuronal injury, can be applied to preparation of the medicine for treating cerebral arterial thrombosis, and has a very good application prospect.

Disclosed are acid-sensing ion channel (ASIC) inhibitors and their use for treating or inhibiting the development of a condition in which inhibiting an ASIC stimulates or effects treatment or inhibition of the development of the condition. More particularly, this invention relates to proteinaceous ASIC inhibitors and their use for treating or inhibiting the development of a neurological condition, neuronal damage, ischaemia, pain, ischaemia-reperfusion injury, a cancer, chronic kidney disease, acute kidney injury, arthritis and retinal detachment. The ASIC inhibitors are also useful for inhibiting damage to an organ during organ transplantation.

Adrenomedullin (ADM) is shown to be protective against damage to neurons as a result of hypoxic brain injuries, radiation brain injuries, and to prevent neurodevelopmental injury in encephalopathy of prematurity; 22q11.2 deletion syndrome, e.g. DiGeorge Syndrome; and other neurologic diseases associated with mitochondrial dysfunction. Modified ADM peptides are provided, which are stabilized relative to the native peptide. In an embodiment, a therapeutic composition is provided, comprising an ADM analog of the disclosure, and a pharmaceutically acceptable excipient. In an embodiment, a method is provided for treating or preventing neurologic damage in an individual, the method comprising administering an effective dose of ADM.

This invention belongs to the field of pharmaceutical technology and discloses arbutin, its polyhydroxy derivatives, their compositions, and uses. Using a microbial transformation method, this invention successfully modified the structure of arbutin, obtaining three novel arbutin derivatives with polyhydroxy substitutions. In vitro neuronal inflammation assays and neuronal oxidative damage protection assays confirmed that these compounds possess good anti-neuroinflammatory and neuronal damage protective activities. Simultaneously, in vivo Alzheimer's disease mouse model experiments demonstrated that these compounds can significantly improve the learning and memory abilities of AD mice, and can serve as active ingredients in drugs for treating neurological diseases. In vitro antitumor cell assays confirmed that compounds I-III possess significant antitumor activity and can serve as active ingredients in antitumor drugs, with broad applications.

There is provided a method of treating or improving a symptom of a neuronal injury in a subject, the method comprising administering to the subject a therapeutically effective amount of an acellular allogenic preparation with exosomes (UCF or UCF-E) wherein the acellular allogenic preparation is derived from pooled human umbilical cord blood.

The invention relates to application of columbianol angelica acid ester in preparation of a medicine for preventing and treating Parkinson's disease, and relates to the technical field of biological medicine. According to the application disclosed by the invention, the columbianidin is used for preparing the medicine for preventing and treating the Parkinson's disease, mitochondria damage of cells of the Parkinson's disease can be alleviated, and oxidative stress damage can be reduced, so that the cell activity is increased, the cytotoxicity is reduced, neuron damage of the Parkinson's disease is reduced, and a protection effect is achieved in neuron damage; the motion symptoms of the Parkinson's disease are improved. The dihydroopisorcinol angelate plays a role in protecting neurotoxicity induced by MPTP and metabolite MPP + thereof, provides a new medicine and method for preventing and treating Parkinson's disease, can be applied to preparation of various neuroprotective medicines, and has a better application prospect.

The application discloses an application of an iPLA2 beta inhibitor in preparation of a medicine for preventing and / or treating zika virus infection, and belongs to the technical field of biological medicine. The iPLA2 beta inhibitor is preferably FKGK18, which can inhibit replication of zika virus in host cells, and reduce virus RNA level and virus protein expression level. Animal experiments show that FKGK18 administration can significantly reduce virus load in brain tissues of infected animals, reduce glial cell activation, and inhibit expression of neuroinflammatory factors, thereby reducing zika virus infection related neuroinflammatory reaction and neuron damage. The application further provides a pharmaceutical composition containing the iPLA2 beta inhibitor, and a scheme of combined use of the iPLA2 beta inhibitor and PE-DHA. The application provides a new drug intervention target and candidate drug for prevention and treatment of zika virus infection and related nervous system damage, and has a good clinical application prospect.

The invention discloses an oxygen supply nutrition delivery micro-fluidic brain organ chip and a preparation method thereof, and belongs to the technical field of biomedical engineering and micro-fluidic organ chips, and the preparation method comprises the following steps: performing oxidative stress treatment on microglial cells, inoculating the microglial cells into an organ culture cavity, and inoculating neurons subjected to hypoxia and ischemia treatment into a peripheral nerve culture cavity; establishing concentration distribution of inflammatory factors or injury related factors through a nutrition mixing matrix and a distribution branch so as to simulate a difference microenvironment between the adjacent end and the far end of a focus; performing time sequence evaluation on the interaction process of microglial cell activation and neuron damage by combining morphological observation and molecular detection; and establishing concentration distribution of inflammatory factors or injury-related factors between the two cavities through a nutrition mixing matrix, and obtaining morphology and molecular readout according to a time sequence of 24-72 hours so as to reproduce the interaction process of microglial cell activation and neuron injury.

This invention discloses the application of a miR-5588-3p inhibitor, belonging to the field of biomedical technology. Studies have found that miR-5588-3p expression is abnormally elevated in the plasma of epilepsy patients. Administration of the miR-5588-3p inhibitor 72 hours before constructing a tree shrew epilepsy model can effectively reduce the seizure severity, seizure rate, and mortality rate in epileptic tree shrews, and alleviate brain pathological damage. The miR-5588-3p inhibitor described in this invention is used to prepare drugs for treating epilepsy, and its nucleotide sequence is as follows: GCUGGCAUUAGUGGGACUU. This invention can effectively reduce the seizure rate and mortality rate in epileptic tree shrews, effectively prolong the clonic latency and seizure latency, shorten the seizure duration, and effectively reduce the seizure severity. The miR-5588-3p inhibitor can significantly reduce hippocampal neuronal damage.

This application relates to the field of biomedicine, specifically to the use of small molecule compounds in the preparation of drugs for the treatment and / or prevention of α-synuclein diseases, wherein the small molecule compounds are selected from at least one of AO-365 / 43264238 and AG-670 / 40728295. The small molecule compounds provided in this invention can precisely target and interfere with α-syn-VAPB interactions, improving neuronal damage caused by abnormal aggregation of α-synuclein, thereby safely and effectively treating and / or preventing α-synuclein diseases, particularly Parkinson's disease.

The present invention relates to a novel association or combination of active ingredients useful in the prevention and repair of neuronal damage, both centrally and peripherally. In greater detail, the present invention relates to an association or combination of an extract of Gastrodia elata, citicoline, L-acetylcarnitine and at least one vitamin of group B. Furthermore, the invention also relates to the pharmaceutical compositions and / or compositions for medical devices and / or nutraceutical and / or food compositions comprising that association and to their use in therapy, in particular in the protection of the functionality of the central and of the peripheral nervous system.

The application discloses a kind of composition and its application, the composition is suitable for such as student group etc. The crowd engaged in high-intensity brain work, can improve the cognitive function decline and nerve injury caused by "chronic sleep deprivation (CSD)". It contains traditional Chinese medicine decoction pieces (according to daily amount) are: prepared 4.5~13.5g rhizoma polygonati, mulberry 4.5~13.5g, medlar seed 4.5~13.5g, longan meat 3~9g, chrysanthemum 3~9g, dried tangerine or orange peel 1.5~4.5g. Its preparation method is: the above-mentioned natural medicine is extracted by water extraction method after being separated or mixed, and the extract is spray dried to prepare powder. The powder is mixed uniformly to prepare the concentrated product. The water extract components have synergistic effect, can significantly alleviate the insufficient sleep caused by long-term passive overtime, and then the cognitive function decline, memory loss and emotional regulation imbalance caused by neuron damage.

The invention discloses a new application of a dried periplaneta americana polypide extract, and relates to the technical field of the dried periplaneta americana polypide extract, and the dried periplaneta americana polypide extract can improve blood circulation and capillary functions of cerebral small vascular diseases through anti-inflammatory, anti-oxidation and tissue repair effects. Meanwhile, neuron damage can be relieved, and the cognitive function can be improved. Animal pharmacological experiment results show that the American cockroach dried polypide extract can significantly improve the cognitive competence of model animals, and has great application value in the field of treatment of cerebral small vascular disease cognitive impairment.

This invention provides the application of a strain of *Lactobacillus reuteri* in the preparation of drugs for the prevention, relief, and / or treatment of cognitive impairment, belonging to the field of neuroprotection and microecological regulation technology. The *Lactobacillus reuteri* strain is designated ATCC 23272; the cognitive impairment is caused by exposure to environmental pollutants. In this invention, colonization of *Lactobacillus reuteri* ATCC 23272 can activate the IAA / AHR / Wnt9a / PLD3 signaling pathway, increase the expression levels of Wnt9a and PLD3 proteins in DEP-exposed mice, effectively restore DEP-induced neuronal damage, and has a certain effect in preventing, alleviating, or treating DEP-induced cognitive impairment.

The invention discloses an intelligent regulation and control system for combined treatment of glioblastoma, and relates to the technical field of intelligent equipment. The intelligent regulation and control system for glioblastoma combined treatment comprises a patient screening module used for acquiring tumor image data and cell cycle data of a patient; the drug delivery module comprises a temozolomide drug delivery unit and an IL-6 receptor antibody drug delivery unit; the biomarker monitoring module is used for detecting a DNA damage marker level, a serum cell factor concentration and a neuron damage marker level in tumor cells of the patient; the data analysis and decision-making module is used for receiving the patient tumor image data and the cell cycle data output by the patient screening module and the detection result output by the biomarker monitoring module, automatically judging a treatment node based on a built-in preset threshold value and sending a regulation and control instruction to the drug administration module; the synergistic administration of the temozolomide and the IL-6 receptor antibody is realized. The system can realize precise treatment of glioblastoma.

The present application relates to the technical field of drugs related to nerve injury caused by heavy metal pollution, and particularly relates to application of a compound for inhibiting ARMC10 phosphorylation in preparation of a drug for antagonizing tin-induced nervous system injury. Exposure of trimethyltin chloride induces mitochondrial dysfunction of nerve cells, and a key mechanism thereof is abnormal phosphorylation of ARMC10 at a serine 43 site. The phosphorylated protein triggers excessive division of mitochondria, collapse of membrane potential and energy metabolism disorder, leading to neuron injury. Based on the above target, a compound for antagonizing tin-induced nervous system injury is screened, the compound can specifically inhibit protein phosphorylation, effectively reverse mitochondrial dynamics imbalance and dysfunction induced by trimethyltin chloride, and reduce neurotoxicity. The technical scheme can solve the technical problem that the prior art lacks an effective drug for antagonizing tin-induced nervous system injury, and the compound has application potential for treating nervous system injury and cognitive dysfunction caused by tin exposure.

The present disclosure relates to recombinant viral vectors, pharmaceutical compositions comprising such recombinant vectors, and methods of preventing and treating Parkinson's disease (PD). In particular, the present disclosure provides adeno-associated virus (AAV) vectors, i.e., AAV-PHPeB, capable of expressing hyaluronate synthase 2 (Has2) within the host brain across the blood brain barrier. The invention provides a method for producing the AAVs, and also provides a method for improving the content of hyaluronic acid (HA) in the brain by expressing Has2 for a long time in the brain so as to remarkably recover neuronal damage and relieve dyskinesia to prevent and treat Parkinson's disease.