121 results about "Neuronal damage" patented technology

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 i) an extract of Gastrodia elata and ii) at least one ingredient selected from the group comprising or, alternatively, consisting of citicoline, L-acetylcarnitine and, preferably, at least one vitamin of group D, and / or mixtures thereof, and / or at least one vitamin of group B, and / or mixtures thereof. Furthermore, the invention also relates to the pharmaceutical compositions and / or compositions for medical devices (Regulation (EU) 2017 / 745) 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 nervous system and in the prevention and / or treatment of central and peripheral neuropathies.

The invention relates to the technical field of biological materials, in particular to a hydrogel scaffold material for spinal cord injury repair as well as a preparation method and application of the hydrogel scaffold material. The hydrogel scaffold material AP39 (AP39-coated LIP) for spinal cord injury repair is prepared by combining the liposome-coated AP39 (AP39-coated LIP) serving as a drug with a GelMA hydrogel scaffold, and a scaffold is provided for injured spinal cords, so that axon regeneration of injured parts is guided, mitochondria of the injured parts is targeted to release H2S, neuronal injury is relieved, and the spinal cord injury repair effect is improved. Therefore, nerve regeneration and functional recovery after spinal cord injury are promoted.

The invention provides an application of a pentacyclic triterpenoid compound targeting hydroxyl steroid 17-beta dehydrogenase 4. The pentacyclic triterpenoid compound can effectively relieve or treat central nervous system diseases (inflammatory diseases), including central nervous system degenerative diseases or chronic central inflammatory diseases. The pentacyclic triterpenoid compound can maintain the structural stability or activity of hydroxysteroid 17-beta dehydrogenase and maintain the stability or activity of peroxisome, thereby relieving or treating central nervous inflammation. The pentacyclic triterpenoid compound can target hydroxysteroid 17-beta dehydrogenase 4, inhibit neuroglial cell excessive activation related neuroinflammation, relieve neuron damage or death speed and improve a central nervous system cell metabolism microenvironment.

The invention discloses application of PGRN in preparation of products for preventing and treating neuropsychiatric disorder related diseases caused by estrogen deficiency. The invention provides an application of a PGRN protein or a coding gene thereof or a virus expressing the coding gene thereof in preparation of a product with any one of the following functions: 1) preventing or treating or saving neuropsychiatric disorder related diseases caused by estrogen deficiency; 2) preventing or treating perimenopausal anxiety and / or depression symptoms; and 3) relieving anxiety-like behaviors and / or depression-like behaviors caused by estrogen deficiency. The application proves that the PGRN can play a role in protecting neuron damage caused by estrogen deficiency by rescuing CTSD enzyme activity and an autophagy pathway, and prompts that related medicines and measures influencing secretion and content of the PGRN can treat perimenopausal anxiety and depressive symptoms; and a new target and a new idea are provided for clinical treatment and drug development of anxiety and depression symptoms of climacteric women.

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 Eucommia lignan in preparation of drugs for preventing and treating sepsis in the technical field of medicines. According to the scheme, the effects of the eucommia ulmoides lignan on the aspects of relieving sepsis inflammatory response, regulating cell phenotype and related protein gene expression, relieving neuron damage and the like are fully verified from the cell and animal levels, and the application value of the eucommia ulmoides lignan in preparation of the medicine for preventing and treating sepsis is proved.

The invention discloses an application of a polypeptide in preparation of a medicine for preventing or treating cerebral apoplexy. The polypeptide comprises an amino acid sequence as shown in SEQ ID NO: 1. The N15 polypeptide expressed by the sequence can inhibit apoptosis and autophagy of damaged neurons by inhibiting expression of Tom20 and PARP proteins, promote expression of SYN-1 protein to promote a patient with ischemic cerebral apoplexy to recover learning, memory and cognitive functions, can comprehensively protect neuronal damage caused by ischemic cerebral apoplexy, can promote recovery of damaged nerve cells of an OGD model, and has a good application prospect. The polypeptide has an obvious protection effect on neuronal cells, the polypeptide is connected with a cell transmembrane carrier and can penetrate through a blood brain barrier to enter brain tissue to directly act on the neuronal cells, and an ischemic cerebral apoplexy animal model verifies that the polypeptide has an effect of treating cerebral apoplexy. Particularly, the cognitive ability and learning and memory ability of a mouse with cerebral arterial thrombosis can be recovered to a normal level, and a good treatment effect on cerebral arterial thrombosis is achieved.

The invention provides application of a probiotic composition in preparation of a medicine for preventing and / or treating Alzheimer's disease, and belongs to the technical field of probiotic medical application. The probiotic composition disclosed by the invention is prepared from lactobacillus rhamnosus, bifidobacterium lactis and bifidobacterium bifidum. According to the probiotic composition disclosed by the invention, on the phylum level, the relative abundance of Verrucomicrobiota (verruca microflora phylum) is improved by the probiotic composition, and the relative abundance of the verrucomicrobiota (verruca microflora phylum) is improved by the probiotic composition; in the level of genus, the probiotic composition increases the relative abundance of the beneficial bacteria genus Akkermansia (Ackermania genus) and Bifidobacterium (Bifidobacterium genus), and in the level of genus Akkermania (Ackermania genus) and Bifidobacterium (Bifidobacterium genus); the behavioral cognition level can be remarkably improved, neuron injury is improved, and intestinal barrier injury is improved.

The invention discloses application of sodium butyrate in preparation of a medicine for relieving brain injury caused by gas explosion, the sodium butyrate regulates nerve cell ferroptosis through a JNK / P38 MAPK pathway to relieve the brain injury caused by gas explosion, firstly, an animal model of rat brain injury caused by gas explosion is established, and the relation between NaB and brain tissue neuron injury is intervened and observed by applying NaB; secondly, a shock wave physiotherapy instrument is used for impacting a co-culture system of three cells of CTX, H19-7 and GMI-R to simulate explosion to construct an in-vitro experimental model, P38, ERK and Fer-1 inhibitors are adopted for intervention, iron metabolism, ferroptosis and MAPK signal channel factor changes are observed from the cell and molecular level, a mechanism for inhibiting ferroptosis through a related cascade signal channel mediated by NaB-mediated intestinal-brain axis regulation and control is clarified, and the effect of inhibiting ferroptosis is achieved. And a theoretical basis is provided for further explaining the action mechanism of the gas explosion brain injury.

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 (20S)-ginsenoside Rh1 in preparation of drugs for preventing and / or improving cerebral arterial thrombosis, and relates to the technical field of medical application of natural drugs. The invention verifies that (20S)-ginsenoside Rh1 up-regulates the expression of an anti-apoptosis gene by promoting STAT3 phosphorylation and translocation to a cell nucleus, so that the (20S)-ginsenoside Rh1 plays a role in protecting neuronal injury induced by sugar oxygen deprivation. In MCAO model mice, the (20S)-ginsenoside Rh1 obviously relieves the symptom of ischemic cerebral apoplexy and has positive influence on neurodegenerative events related to cerebral infarction, and the anti-apoptosis and neuroprotection effects are most prominent. Mechanism research shows that (20S)-ginsenoside Rh1 plays a therapeutic role in PC12 cell and MCAO model mice by activating a JAK2 / STAT3 signal channel.

The present disclosure provides methods to detect and optionally quantify Nfl present in cerebrospinal fluid and blood and use of the methods to detect and optionally measure levels of Nfl biomarkers indicative of neuronal damage. Also disclosed are anti-Nfl antibodies.

The invention discloses a strain for preventing and treating Parkinson's disease as well as a composition, application and a product thereof, and relates to the technical field of microorganisms. The invention provides three strains from human milk, namely lactobacillus helveticus LV-20, plant lactobacillus LPP8 and lactobacillus fermentum PL-15, the invention further provides a composition capable of preventing and treating the Parkinson's disease, and the three strains can well prevent and treat the Parkinson's disease and can be used for preventing and treating the Parkinson's disease. The composition can significantly improve dyskinesia (such as static tremor, muscle stiffness, movement retardation, posture balance and the like), reduce neuron damage, significantly reduce alpha-syn deposition, reverse sensory function degradation and cognitive disorder, relieve sleep disorder, inhibit neuroinflammation and oxidative stress, reduce and repair intestinal barrier damage, relieve gastrointestinal dysfunction, and improve the curative effect. As probiotics or synbiotics, products for treating and preventing Parkinson's disease have a wide application prospect.

The invention discloses an application of NeuroD1 (NeuroD1) in repairing Alzheimer's disease (Alzheimer's disease). The invention also discloses an application of the carrier for coding NeuroD1 in any one of the following aspects: preventing neuron damage and apoptosis; hippocampus atrophy is inhibited; the neuroinflammation is relieved; repairing blood vessel / blood brain barrier injury; the AD biomarker level of the cerebrospinal fluid is recovered to be normal; the removal of pathological toxic proteins in brain tissues is promoted; glucose metabolism is improved; the space working memory ability is enhanced; and regenerating neurons.

The invention discloses application of lactobacillus muricatum in preparation of a medicine for preventing and / or treating depression in the technical field of microorganisms, and the lactobacillus muricatum is preserved in the China Industrial Microbiological Culture Collection Center (CICC) with the preservation number of CICC23140. Research finds that lactobacillus muricatum which is preserved in the China Industrial Microbiological Culture Collection Center and has the preservation number of CICC23140 has a good effect of improving and / or preventing and / or treating cortisol-induced depression, and inactivated lactobacillus muricatum can effectively prevent hippocampal neuron damage, reduce expression of inflammatory factors in the brain, prevent and treat cortisol-induced depression, and can be used for preventing and treating cortisol-induced depression. Not only can the anxiety symptom of depression be improved, but also dyskinesia can be relieved.

The invention discloses an experimental material for constructing a cerebral microcirculation disturbance Parkinson's disease animal model and application of the experimental material, and belongs to the technical field of animal model construction. The invention particularly relates to an experimental material for constructing a model, application of the experimental material, a model construction method and application of the model. Research finds that cerebral microcirculation disturbance can cause increase of blood brain barrier permeability, and neuronal damage aggravation caused by penetration of a large amount of inflammatory factors in systemic circulation into the brain; meanwhile, glial cells at the nerve and blood vessel coupling position are activated, tight connection between endothelial cells is damaged, and excessive active oxygen is generated, so that apoptosis of dopaminergic neurons is further aggravated. The research on the Parkinson's disease by adopting the microcirculation disturbance animal model is more in line with the actual pathophysiological environment of the Parkinson's disease patient, and the experimental result has higher reference value.

This invention discloses the application of the inflammasome NLRP6 as a target in screening drugs for treating epilepsy, and the application of NLRP6 expression inhibitors in the preparation of drugs for treating epilepsy. This invention reveals for the first time the role of the inflammasome NLRP6 in epileptic neuroinflammation. This invention identifies NLRP6 as a key regulator of neuroinflammation in epilepsy and investigates its role in activating the caspase-1 / IL-1β / IL-18 signaling pathway. Knockdown of NLRP6 can improve the damaging effects of epilepsy on neurons, thereby improving seizures; overexpression of NLRP6 may exacerbate seizures, neuronal damage, and neuroinflammatory responses. This invention provides a new potential target for epilepsy treatment, offering new research ideas and directions.

The present invention relates to the technical field of biological medicines. Disclosed are a combined detection kit for assisting in diagnosis of Alzheimer's disease and the use. Disclosed is the combined use of at least four of amyloid β-proteins, phosphorylated Tau proteins, biomarkers of neurodegeneration or neuron damage, and biomarkers related to neuroimmune disorder, synaptic dysfunction and blood brain barrier alternation in assisting in diagnosis of Alzheimer's disease. Compared with single-biomarker detection existing in the market and the combined detection using a small number of markers disclosed in some published patents, the marker combined detection provided by the present invention achieves a higher specificity or sensitivity. The present invention establishes a brand-new algorithm model, and both AD scale rating and brain function imaging diagnosis result rating are incorporated into the algorithm model for cooperative diagnosis; under the condition of a 95% specificity, the diagnosis sensitivity thereof can reach 95%, which is far higher than that of similar products in the market.

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.

The present invention relates to the field of medicine, and specifically to the use of taraxasterol or its salts in the preparation of drugs for preventing or treating traumatic brain injury. Animal experiments have confirmed that the taraxasterol of the present invention can improve the motor ability of the balance beam experiment in the neurological function score of mice with brain trauma, improve the neurological function scores including motor tests and sensory tests; reduce the permeability of the blood-brain barrier, reduce brain edema, improve the short-term lesion volume after traumatic brain injury, and inhibit microglial activation and immune cell infiltration. Cytological experiments have confirmed that taraxasterol can reduce microglia-mediated neuroinflammation, reduce the expression of inflammatory factors such as TNF-α, IL-6, and IL-1β, and reduce neuronal damage.

The invention relates to sulfonylurea derivatives and medical application thereof. Specifically, the invention relates to a sulfonylurea derivative shown in a general formula (I), a preparation method of the sulfonylurea derivative, a pharmaceutical composition containing the sulfonylurea derivative and application of the sulfonylurea derivative in treatment of diseases and symptoms affected by neuronal injury, such as cerebral apoplexy, cerebral injury, neuropathic pain, migraine, inflammatory pain, chronic pain or depression. The definition of each group in the general formula (I) is the same as that in the specification. # imgabs0 #

The invention discloses an application of a compound RH-1402 in preparation of an antidepressant drug, belongs to the field of medicines, provides an application of the compound RH-1402 in preparation of the antidepressant drug, and particularly proves that the compound RH-1402 can effectively improve depression-like behaviors of mice, alleviate the level of inflammation in the brain and improve neuron damage through animal experiment results, so that the compound RH-1402 can be used for preparing the antidepressant drug. The action mechanism is related to the inflammation level in the hippocampus, and the application prospect is wide.

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.

The present invention relates to a sulfonylurea derivative and medical uses thereof, specifically relating to the sulfonylurea derivative shown in general formula (I), a preparation method thereof, a pharmaceutical composition containing same, and a use of same for treating diseases and disorders affected by neuronal damage, for example: cerebral stroke, brain damage, neuropathic pain, migraines, inflammatory pain, chronic pain, or depression. The definition of each group in the general formula (I) is the same as that in the description.

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 invention discloses a method for constructing a frontotemporal lobe degeneration animal model by using TAF15 prefabricated precursor fibers, and belongs to the technical field of biology. The TAF15PFs provided by the invention is formed by aggregation of protein fragments with an amino acid sequence as shown in SEQ ID NO.1, and can promote aggregation of TAF15 protein in the brain, induce neuronal injury and synaptic dysfunction, and lead to cognitive dysfunction and anxiety and depression-like behaviors of mice. The TAF15PFFs is injected into the prefrontal cortex of a mouse, so that the frontal-temporal lobe degeneration mouse model can be constructed. The invention provides a new animal model for pathogenesis research and therapeutic drug screening of frontotemporal lobe degeneration.

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.