57 results about "Neuron apoptosis" patented technology

The present invention provides a method for improving respiratory function and inhibiting muscular degeneration (e.g., dystrophy and atrophy). Alternative embodiments of the invention provide a method of inhibiting motor neuron apoptosis and the subsequent muscular degeneration associated with the denervation of muscular tissue resulting from neuron death.

The present invention provides a method for improving respiratory function and inhibiting muscular degeneration (e.g., dystrophy and atrophy). Alternative embodiments of the invention provide a method of inhibiting motor neuron apoptosis and the subsequent muscular degeneration associated with the denervation of muscular tissue resulting from neuron death.

Provided are methods for protecting against or reducing neurotoxicity of exposure to a neurotoxic agent, comprising administering an electrokinetically altered aqueous fluid as provided herein in an amount sufficient to provide for neuroprotection against the neurotoxic agent, preferably where protecting against or reducing loss of motor coordination in the subject exposed to the neurotoxin is afforded. In certain aspects, protecting or reducing neurotoxin-mediated neuronal apoptosis is afforded, and / or activating or inducing at least one of PI-3 kinase and Akt phosphorylation in neurons is afforded. Preferably, administering the fluid comprises administering the fluid prior to exposure to the neurotoxic agent. Additionally provided are methods for preserving or improving motor coordination in a subject having a neurodegenerative condition or disease, comprising administering an electrokinetically altered aqueous fluid as provided herein in an amount sufficient to provide for preserving or improving motor coordination in the subject.

The invention discloses a micro-molecule polypeptide TAT-p53DM and an application thereof to preparing a medicine for treating or preventing ischemic stroke. A fusion protein polypeptide TAT-p53DM of a TAT protein transduction domain and p53DM is artificially synthesized; TAT carries p53DM protein polypeptide to pass through a blood brain barrier through blood so as to be taken by nerve cells; used in an in-vitro and in-vivo ischemic stroke model, the micro-molecule polypeptide TAT-p53DM is capable of effectively playing a biological role in blocking binding between death domain of death associated protein kinase 1 (DAPK1DD) and tumor suppression protein p53DNA binding motifs (p53DM), inhibiting signals capable of causing neuronal apoptosis and necrosis at DAPK1 downstream, and reducing ischemic stroke brain injury; moreover, molecular targets are provided for further developing medicines for clinically treating ischemic stroke.

The present invention relates to use of small RNA molecule, is especially use of miRNA-34a, and belongs to the field of biomedicine material technology. By means of Northern process and other process, miRNA-34a is determined to be the age related expression, and by means of the contrast to the prefrontal lobe cortical tissue miRNA' s of rats in different age sections, it is found that the expression of miRNA-34a in the pallium of rhesus and the prefrontal lobe cortex of rat exhibits age dependent change. The present invention establishes a rat neuron AD cell model for the research of possible action mechanism of miRNA-34a. By means of further transfecting miRNA-34a precursor, miRNA-34a antisense RNA and other contrasts, it is found that miRNA-34a possesses neuron apoptosis effect of antagonizing A-beta induction.

The present invention discloses achyranthes bidentata polypeptide, a production method and applications, and the achyranthes bidentata polypeptide is produced with the steps including polypeptide extraction, polypeptide separation, etc. The achyranthes bidentata polypeptide is used to the preparation of drugs and health products for treating peripheral nerve injuries, cerebrovascular accidents, ischemic brain injuries, cerebral traumas, optic nerve injuries, spinal cord injuries and central nervous system injuries, antiaging and preventing neurodegenerative diseases. Experiments prove that the extracted achyranthes bidentata polypeptide (protein) of the present invention has the effects of promoting the growth of nerves, preventing the fading of nerve cells and promoting the regeneration of injured nerves, the source of medicinal materials is single, the preparation method is advanced, the technique is reasonable, the ingredients of preparations are definite, safety is high, and pharmacological action is obvious.

This invention provides a method for treating Parkinson's disease (PD), particularly early stage of PD by orally administering to a mammal sporoderm-broken germination activated Ganoderma lucidum spore powders (GASP) to reduce and / or release the symptom of rotatory behavior in PD, to reduce the progression of neuron apoptosis and to improve the tyrosine hydroxylase (TH) activity so as to increase the conversion of hydroxydopamine (DOPA) to dopamine in the dopaminergic neurons. This invention also provides a method for reducing neuron apoptosis and a method for improving TH activity in dopaminergic neurons by orally administering to a mammal GASP.

The present invention relates generally to methods for inhibiting neuron apoptosis and necrosis associated with excess glutamate release.

The invention discloses an application of imatinib mesylate in preparation of drugs for resisting Parkinson's disease (PD). The application of imatinib mesylate (STI571) in preparation of drugs for treating neurodegenerative diseases belongs to the protective range of the invention, and the neurodegenerative diseases can be PD. An experiment proves that by continuous administration of the STI571, the dyskinesia induced by MPTP can be obviously improved, and the cognitive dysfunction of mice can be improved. The STI571 can obviously improve the dopaminergic neuron loss induced by the MPTP, can inhibit the rat CA1 and DG (diacylglycerol) region nerve cell apoptosis reaction induced by rotenone, can obviously inhibit the primary substantia nigra neuron apoptosis and Lewy protein expression induced by rotenone, and can inhibit the phosphorylation activation of PKC (Protein Kinase C) and Akt. The STI571 used as a specific inhibitor of c-Ab1 can resist the formation of PD, can improve the behavioral abnormity and cognitive dysfunction of PD, can be used as a new candidate drug for resisting neurodegenerative diseases such as PD and the like, and has favorable application prospects; and the clinical indications of the STI571 are greatly expanded.

The invention relates to an apparatus for treating a bodily lesion that is associated with inadequate blood perfusion, partial denervation, neuronal apoptosis, tissue loss, pain, oedema and / or infection. The inventive apparatus is used to apply external, non-invasive, analgesic electromagnetic fields (EMF) to the patient with the lesion, in an area removed from the site of the lesion. The aforementioned electromagnetic fields are effective in increasing angiogenesis, vasculogenesis, neural tissue regeneration and osteogenesis, restoring the wound repair process, providing analgesic, anti-oedema, anti-inflammatory effects and / or repairing wounds. The electromagnetic fields include frequencies from several Hertz up to less than approximately 300 Hz, as well as components of a static field from between several microteslas and a maximum intensity of between approximately 0.3 and approximately 0.8 mT, which can be applied alone or together with a homogeneous static field from approximately 40 to approximately 80 T, or approximately 400 to approximately 800 Gauss.

The invention discloses an application of cholest-4-ene-3,6-dione in preparing a drug for treating or preventing neuron injury. Cholest-4-ene-3,6-dione can relieve hippocampus neuron oxidative stressinjury caused by glutamic acid, cerebellar granule neuron apoptosis injury caused by potassium deprivation and cortical neuron and cerebellar granule neuron oxidative stress injury caused by glutamicacid, also has a function of remarkably reducing infarct volume in an MACO (middle cerebral artery occlusion) model of a stroke rat and has the potential of a neuroprotective agent used for being developed into multiple acting mechanisms. Neurodegenerative diseases such as the Parkinson's disease, the Alzheimer's disease, the tau protein disease, amyotrophic lateral sclerosis and the like as wellas cerebral stroke, cerebral injury and spinal cord injury are all caused by neuron injury, and neuron injury is further aggravated. Cholest-4-ene-3,6-dione has a protection function on neuron injuryand has potential functions in drugs for treating or preventing neuron injury.

The invention relates to a method for preparing achyranthes extractive, which comprises that using 0-95% alcohol solution to extract the achyranthes for 1-3 times, combining the extractives, using gel post chromatography to separate and purify, freezing and drying the eluent, to obtain the product, which can be used to prepare the drug for treating cerebral apoplexy, optic nerve hurt or the like. The invention has high safety, significant drug effect, and wide application.

Provided is a pharmaceutical composition for inhibiting apoptosis of neurons or neurodegeneration. The pharmaceutical composition effectively prevents or treats diseases related to apoptosis of neurons or neurodegeneration.

The invention discloses an application of oxymatrine in medicines for treating neonatal hypoxic ischemic brain damages. An experiment result shows that oxymatrine has a certain dose-effect correlation when used in a safe dose range; when the dose is 120mg / kg of body weight, the volume of ischemia area cerebral infarction and neuron apoptosis rate can be reduced; pathological damages to brain tissues can be relieved; the activity of antioxidase in the brain tissues can be improved; and the content of malondialdehyde is lowered. The oxymatrine has the effects of preventing injuries and deaths caused by neonatal hypoxic ischemic brain damages and promoting neural functional recovery.

The invention belongs to the technical field of medicine, and specifically relates to applications of basic fibroblast growth factor (bFGF) in preparation of drugs for treatment of spinal cord injuries, wherein the spinal cord injuries comprise spinal cord primary injuries and spinal cord secondary injuries caused by various factors. According to the applications of the bFGF in preparation of the drugs for treatment of spinal cord injuries, the form of the drugs can comprise a powder injection, a water agent, a liposome, and the like. With the bFGF, endoplasmic reticulum stress can be inhibited, and spinal cord neuron apoptosis caused by endoplasmic reticulum can be reduced so as to provide a treatment effect for spinal cord injuries.

The invention discloses application of DPP4 inhibitors to preparation of drugs used for preventing and treating epilepsy, belonging to the field of medical application. The DPP4 inhibitors are applied to prolong the incubation period of epilepsy of rats, shorten duration time of epilepsy, reduce the grade of attack, lower the amplitude and frequency of abnormal discharge of nerve cells, alleviate neuronal damage of rats with epilepsy, improve neuronal apoptosis of rats with epilepsy, and decrease neuronal degeneration and necrosis of rats with epilepsy. The DPP4 inhibitors in the invention are approved clinical medicines; and the DPP4 inhibitors are definite in active ingredients and curative effect, low in toxic and side effect and long in duration time of drug effect and can reduce cost for research and development of the drugs.

The invention relates to the technical field of medicine, in particular to an application of a bFGF (basic Fibroblast Growth Factor) to preparation of a medicament for treating human ischemic stroke. During the application of the bFGF (basic Fibroblast Growth Factor) to preparation of the medicament for treating human ischemic stroke, the medicament can be in the forms of a powder injection, a water aqua, a lipoplast and the like. The bFGF can be used of treating ischemic stroke; and a small dosage of bFGF can be used for inhibiting endoplasmic reticulum stress, reducing neuronal apoptosis caused by endoplasmic reticulum, and has a treatment effect on ischemic stroke.

The invention is designed to provide lobeline applied for preparing medicine used for curing neuron apoptosis. The invention also relates to the applications of the lobeline for curing a CNS degenerative disease medicine. The lobeline up-regulates the concentration of synapse intermission DA by inhibiting the transport of DAT, so the apoptosis speed of a nerve cell can be stopped or retarded with little adverse effect. The lobeline is proved that the lobeline can protect dopaminergic neuron, so the invention provides the new medicine used for the clinical treatment of the CNS degenerative disease.

The invention discloses a micro-molecule polypeptide as well as application and a product thereof. The experiment proves that the micro-molecule polypeptide is applied to preparing medicines for reducing neuronal death after ischemia, medicine for reducing neuronal apoptosis after ischemia and medicines for controlling ischemic stroke and has good effects and actual operational feasibility. According to the product provided by the invention, the active ingredients comprise the medicines for controlling ischemic stroke in the micro-molecule polypeptide, and the medicines refer to medically acceptable dosage forms, preferably injections.

The invention provides application of atractylenolide in preparation of an antidepressant drug, and relates to the field of medicine. In-vitro activity tests prove that atractylenolide I and atractylenolide III have the better protection activity on corticosterone-damaged PC12 cells, and the mechanism is related to inhibition of neuron apoptosis; in-vivo test results show that atractylenolide I and atractylenolide III can significantly shorten the immobility time of a mouse forced swimming test and a mouse tail suspension test. Experiments prove that atractylenolide I and atractylenolide III have the significant antidepressant effect and can be used for preparing the drug for preventing and treating a depressive disorder.

The invention discloses a medicinal and edible dual-purpose composition for preventing and treating vascular dementia and a preparation method thereof, belonging to the fields of food therapy and preparation of health products and traditional Chinese medicines. An optimal dosage form of a composition product is a soft capsule dosage form, and the medicinal and edible dual-purpose composition comprises the following components in parts by weight: 10-18 parts of a seabuckthorn seed procyanidine extract, 4-11 parts of a seabuckthorn flavone extract, 8-18 parts of a longstamen onion bulb extract and 63-72 parts of seabuckthorn seed oil. A preparation method of a soft capsule comprises the following steps: firstly preparing inclusions in the capsule into oil powder suspensions, and then preparing the oil powder suspensions into the soft capsule dosage form. The components of the medicinal and edible dual-purpose composition are all medicinal and edible dual-purpose varieties, are safe, and can be taken for a long time. The medicinal and edible dual-purpose composition disclosed by the invention can be used for effectively reducing the platelet aggregation rate and blood viscosity and increasing the cerebral blood flow, has extremely strong free radical removal and anti-oxidation effects, can be used for reducing the generation rate of MDA, repairing and protecting cranial nerve injury, and inhibiting hippocampal neuronal apoptosis, and plays roles in effectively preventing vascular dementia and treating vascular dementia.

The invention discloses an application of Matrine in preparation of medicine for treating cerebral arterial thrombosis. The experiment result shows that when the Matrine is used within a safe dose range and the dosage is 30 mg / kg bodyweight, certain dosage-efficacy correlation is shown, the volume of cerebral infarction in an ischemia area and the hippocampal neuron apoptosis rate can be reduced, autonomic dysfunction of the focal cerebral ischemia model of a mouse is remarkably relieved, the pathological injury of brain tissue is relieved, the activity of antioxidant enzyme in the brain tissue is improved, and the content of malonaldehyde is reduced. The Matrine has the functions of controlling incidence of cerebral arterial thrombosis, reducing disability and death caused by brain stroke and promoting neural functional recovery.

The invention discloses medical application of a catalpol and / or radix astragali seu hedysari extraction solution. Experiments show that the catalpol and / or radix astragali seu hedysari extraction solution can be used for preventing and treating or delaying motor neuron diseases and nerve injury. Results show that through injection of a catalpol injection solution, a radix astragali seu hedysari injection solution or a composition of the catalpol injection solution and the radix astragali seu hedysari injection solution, the occurrence time of amyotrophic lateralizing sclerosis can be delayed, the survival time can be prolonged, and the limb movement function can be obviously improved. The catalpol and / or radix astragali seu hedysari extraction solution has the effects of resisting shrinkage of spinal anterior horn motor neuron cells, maintaining or activating the growth state of the spinal anterior horn motor neuron cells, resisting neuronal apoptosis and protecting the neurons, has an effect of gaining weight, and also has a high curative effect on the traumatic type nerve injury; meanwhile, the effective components of the catalpol and / or radix astragali seu hedysari extraction solution can be extracted from the traditional Chinese medicines; the used medicines are low-cost and easily available; the catalpol and / or radix astragali seu hedysari extraction solution has a good market prospect.

The invention relates to application of CART (Cocaine Amphetamine Regulated Transcript) in preparing medicaments for treating alzheimers diseases. In the invention, CART is prepared into injection preparations for treating alzheimers diseases, and the defects of the traditional medicaments for enhancing cholinergic action and N-methyl-D-aspartic acid (NMDA) receptor antagonists are overcome. The novel medicament has multiple target point actions on the generation and the degradation of A beta as well as the influence of the neurotoxicity and the molecular mechanism of the A beta. The invention has effects on effectively treating dementia with estrogen and up-regulating intracephalic CART; more CARTs are distributed in intracephalic hippocampus; CART exists in intracephalic acetylcholine neurons and can promote the release of acetylcholine; and mitochondrial dysfunction induced by A beta neurotoxicity is the main pathway for the A beta to cause neuronal apoptosis. The CART has a directaction on mitochondrial succinodehydrogenase subunit B and can maintain the respiration of mitochondria and the generation of energy, alleviate oxidative stress, stabilize mitochondrial membrane potential and prevent the mitochondria from being damaged, thereby inhibiting apoptosis.

The invention discloses a preparation method of a directional EPC (endothelial progenitor cell) sample cell. The preparation method comprises the following steps: S1, collecting fat, and separating fat cells; S2, culturing the fat cells by virtue an ADSCs (adipose derived stem cells) culture medium to obtain a P2-generation ADSCs; and S3, culturing the P2-generation ADSCs by virtue of an EPCs (endothelial progenitor cells) culture medium to obtain a directional EPC sample cell. The directional EPC sample cell, the preparation method and the application have the beneficial effects adipose-derived stromal cells (ADSCs) are pre-induced for three days by adopting an endothelial progenitor cells culture medium to obtain heterogeneous CEL (committed EPC-like) with CD133 expression of 47.63+ / -12.50 percent and vWF expression of 31.10+ / -5.32 percent, and the CEL can increase the blood supply of an injured part, can alleviate ischemic symptom, and is not only beneficial for the structural restoration of an injured area, but also beneficial for alleviating the functional injury of a neurological function; and the CEL restores the blood supply by rebuilding a tissue structure of the injured area, thereby inhibiting the infection environment, reducing the neuronal apoptosis, promoting axonal regeneration and synaptic connection, and restoring partial feeling and movement function.

The invention provides shRNA for inhibiting expression of long-chain non-coding RNA MALAT1. The shRNA is designed for sites 286, 743, 1048 and 4807 of a MALAT1 transcript sequence NR_002847.3 in Genbank or corresponding sites in other transcript sequences. The invention further provides a corresponding plasmid, a lentivirus, a pharmaceutical composition and application of the pharmaceutical composition in treatment of cognitive impairment. The MALAT1-shRNA interference plasmid disclosed by the invention can be used for remarkably and specifically inhibiting the expression of MALAT1 in hippocampal neurons, promoting the process of a neuronal cell cycle and inhibiting neuronal apoptosis and the expression of apoptosis key proteins, so that the effect of resisting stress-induced neuronal cell injury is achieved.

The invention discloses an application of a micromolecular polypeptide for inhibiting neuron apoptosis. According to the application, the micromolecular polypeptide with an amino acid sequence represented by SEQ ID No. 1 shown in the description is prepared through reforming and synthesizing a Glis2 structure; meanwhile, a rat model with intracerebral hemorrhage is modeled, the synthesized micromolecular polypeptide serves as a therapeutic drug for rat intracerebral hemorrhage, PBS serves as a blank control, the micromolecular polypeptide serves as a treatment group, shown by treatment on intracerebral hemorrhage, after being treated by the micromolecular polypeptide, the kinetism of the rat with intracerebral hemorrhage is recovered, the limb reflecting power is obviously increased, the quantity of macrophage activated and the expression level of inflammatory factors are obviously inhibited, and the quantity of nerve tissue cells subjected to apoptosis is reduced.

The present invention relates to a pharmaceutical composition for preventing or treating neonatal hypoxic ischemic encephalopathy (HIE), comprising a thrombin-treated stem cell or an exosome derived therefrom as an active ingredient, and a method for producing the same. According to the present invention, the thrombin-treated stem cell or the exosome derived therefrom has an increased expression of growth factors, immunoregulatory factors, antioxidant factors, or regeneration factors compared to a group not treated with thrombin and also enhances a neuronal apoptosis inhibitory effect, and thus has an advantage in that the therapeutic effect thereof on neonatal hypoxic ischemic encephalopathy (HIE) is excellent.

The invention provides an application of 6-hydroxy-1-hydro-indazole in preparation of medicine for preventing and treating neurodegenerative disease. An action mechanism of the medicine for preventing and treating neurodegenerative disease is characterized in that 6-hydroxy-1-hydro-indazole can inhibit a phosphorylation process of Tau protein, a hyperphosphorylation state of Tau can be alleviated, neuronal apoptosis can be prevented, so that a purpose for preventing and treating neurodegenerative disease can be reached. The application of 6-hydroxy-1-hydro-indazole in preparation of medicine for preventing and treating neurodegenerative disease can effectively inhibit the phosphorylation level of Tau protein and prevent neuronal apoptosis, the action target is clear, so that the therapeutic effect is definite and obvious.

The invention relates to the use of AR-AO14418 in preparing medicament for preventing and treating nerve retrogression diseases, wherein the medicament comprises AR-AO14418 and medically acceptable auxiliary materials, wherein the AR-AO14418 can be bonded with the ATP bonding points of the GSK-3 beta, inhibiting GSK-3 beta activity, and preventing hepatocyte nerve.