99results about How to "Reduced infarct volume" patented technology

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor—neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

This invention relates to methods for treating or preventing an infarction by administering to a patient in need thereof a compound capable of suppressing the expression or activity of the von Willebrand Factor (VWF). Thus, the invention relates to the use of a pharmaceutically effective amount of a VWF inhibitor, such as ADAMTS13, for the preparation of a medicament for treating conditions known to involve infarction to reduce or eliminate the symptoms and effect of an infarction.

The present invention relates to 2-hydroxy-alkylamino-benzoic acid derivatives and to a combination of cell necrosis inhibitor and lithium, process for the preparation of the derivatives or the combination, pharmaceutical formulation containing the derivatives or the combination, and use of the derivatives or the combination by either concomitant or sequential administration for improvement of treatment of neuronal death or neurological dysfunction. The derivatives and the combination of the present invention are useful for treating neurological diseases, such as amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease), spinal muscular atrophy, Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke, traumatic brain injury or spinal cord injury; and for treating ocular diseases such as glaucoma, diabetic retinopathy or macular degeneration.

The present invention is based on the discoveries that PAN-811 (1) reduces infarct volume, suppresses brain edema and decreases mortality associated with ischemia; (2) blocks veratridine-induced swelling and neuronal cell death; (3) chelates free calcium and inhibits MMP-9 activity; and (4) blocks calcium-induced neuronal cell death and suppresses glutamate-induced calcium influx into neuronal cells. More particularly, the present invention relates to methods for treating, ameliorating or preventing vasogenic and/or cytotoxic brain edema, by administering to a subject in need thereof certain thiosemicarbazone compounds or pharmaceutically acceptable salts thereof. An example of such a thiosemicarbazone is 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (PAN-811).

This invention discloses the uses of IL-22 in the treatment and prevention of a nerve damage disease or a neurodegenerative disease. In particular, the invention discloses the uses of IL-22 or IL-22 dimers as follows: (i) can protect neurons to recover the functions of injured neurons after ischemic nerve damage in animals in vivo, thus enabling effective treatment of nerve damage diseases, (ii) can significantly inhibit the loss of dopaminergic neurons in substantia nigra in PD model animal, enhance the functions of dopaminergic neurons, significantly reduce neuronal apoptosis in hippocampus, improve learning and memory capacity of AD model rats, and effectively prevent neuronal loss, thereby enabling more effective treatment of neurodegenerative diseases.

The invention relates to the field of Chinese medicaments, in particular to a Chinese medicinal composition for preventing and treating ischemic brain injury, and a preparation method thereof. The Chinese medicinal composition for preventing and treating ischemic brain injury is an orally taken preparation prepared from extracts of raw astragalus roots, panax notoginseng, kudzuvine roots, baikal skullcap roots and gardenia serving as main active components, as well as pharmaceutical auxiliary materials. The preparation has obvious therapeutic effects on cerebral infarction convalescent symptoms of which the clinical manifestations are eye-mouth distortion, glossolalia, slobbering or hemiplegia, dark red tongue or yellow greasy tongue coating, weak or uneven pulse and the like.

The invention discloses an injection of anemarrhena extractive, which includes the various dosage types of powder injection, small injection, glucose fluid infusion and sodium chloride fluid infusion, wherein the main active constituent of anemarrhena extract includes anemarrhena saponin B-II, anemarrhena saponin E1, anemarrhena saponin B by the weight ratio of 78-92 : 2-12 : 0-6.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia. The treatment was effective when applied either before, or one hour after, the onset of excitotoxicity in vitro and cerebral ischemia in vivo. This approach prevents negative consequences associated with blocking NMDAR activity and constitutes practical therapy for stroke.

The invention relates to novel use of methylene blue (MB) in prevention of acute cerebral ischemia. MB can remarkably reduce cerebral ischemia infarction caused by permanent middle cerebral artery occlusion (middle cerebral artery occlusion MCAO) and alleviate damage of neurological function. The inventors of the invention permanently occlude middle cerebral artery of a mouse by adopting a suture method and after intraperitoneal injection of MB at the moment and at different time points after cerebral ischemia, changes on degree and ethology of permanent cerebral ischemia infarction of the mouse are observed. Researches discover that MB can remarkably reduce infarct volume caused by cerebral ischemia and improve the active ability of the mouse after cerebral ischemia. Through the method provided by the invention, moderate doses of MB are delivered for many times after cerebral ischemia can remarkably alleviate damage degree after permanent cerebral ischemia of the mouse so as to improve the active ability of the mouse after cerebral ischemia. The use of MB is expected to provide a rescue therapeutic measure to cerebral apoplexy and alleviate permanent neurological function deficit after golden treatment period.

The invention relates to the medical field, discloses applications of racemes of pinocembrin, racemes of pinocembrin salt, racemes of pinocembrin precursors or racemes of pinocembrin hydrate in preparation of medicals for preventing and treating cerebral apoplexy, and further discloses the application of racemes of pinocembrin in prevention and treatment of acute ischemic stroke.

An application of L-serine in preparing the slow-release or release controllable medicines in the form of solid, liquid, or spray for treating cerebral ischemia is disclosed.

The invention discloses a preparation method of a metal organic framework material for treating cerebral arterial thrombosis. The preparation method comprises the following steps: step 1, preparing the metal organic framework material; step 2, removing unreacted raw materials and solvent molecules in the metal organic framework material, and activating the metal organic framework material; and step 3, carrying out dopamine modification on the obtained metal organic framework material. The metal organic framework material has superoxide dismutase (SOD), oxygen free radicals can be effectively converted into water and oxygen, meanwhile, the novel metal organic framework material can up-regulate the activity of endogenous antioxidant enzyme of nerve cells, and free radicals are further removed. The metal organic framework material is delivered in the stroke mouse in a lateral ventricle injection mode, the focus microenvironment is improved, the nerve cell death rate is reduced, the infarct volume is reduced, and the mouse postoperative behavioral function is effectively recovered.

The invention provides application of PR-957 in preparing drugs for treating cerebral ischemia-reperfusion injury. The technical scheme is that an MCAO animal model is taken as an experimental subjectand the role of immune proteasome in cerebral ischemic stroke is investigated by using the PR-957. The experimental results show that PR-957 therapy leads to lowering transcription level in ROR gammat and IL-17 by reducing the phosphorylation level of STAT3, so that Th17 differentiation is inhibited, cerebral inflammatory response is reduced, cerebral infarction volume is reduced and neurological dysfunction is alleviated. Therefore, the PR-957 plays a key role in regulating the inflammatory state of helper T cells of the cerebral ischemic stroke in mice and can be used as a therapeutic means of relieving brain injury of the cerebral ischemia-reperfusion injury.

The invention relates to healthcare beverage and a preparation method thereof. The healthcare beverage has functions on assisting the adjustment of blood fat and blood pressure. Salvia miltiorrhiza bge.f.alba and hawthorn are adopted as raw materials, and the beverage comprises the following compositions by weight ratio: 10 parts of salvia miltiorrhiza bge.f.alba, 5 parts of hawthorn, 1 part of crystal sugar, 1 part of honey, 100 parts of purified water and 0.02 percent of p-hydroxybenzoate (g.ml<-1>). The healthcare beverage has simple formula, is convenient to take, has a remarkable effect, and is suitable for the flavor of a particular group of people and satisfies the requirement on adjusting the function of the human body.

The present invention provides a method for treating brain injury or stroke in a subject in need thereof, comprising implanting a microdialysis probe into the injury or insult core of the subject and perfusing the probe with an oncotic agent dissolved in a physiologically acceptable buffer, wherein the microdialysis probe comprises a dialysis membrane with a molecular weight cutoff less than the molecular weight of the oncotic agent.

The invention relates to application of nicotinamide adenine dinucleotide as an active ingredient in preparation of a drug for preventing or treating heart ischemic injuries. In experiments, caudal vein normal saline injection and a heart ischemia operation are carried out on rats in a control group, it is found through research results that a great number of apoptosis signals (TUNEL positive signals) appear on the hearts, while apoptosis signals of rats, on which caudal vein NAD+solution injection is carried out, in an experiment group can be effectively reduced.

The present invention relates to a phenylquinolinone-based and flavone-based derivative and a preparation method thereof, wherein the derivative is a histamine H3 receptor antagonist, can protect andrestore the normal function of central nervous system, especially can be used in neurodegenerative diseases and ischemic brain injury, and has great clinical application value.

Methods for preconditioning and/or providing neuroprotection to the animal central nervous system against the effects of Huntington's disease. Therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and/or copper such as iron chelators, copper chelators, and antioxidants. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). An effective amount of DFO may be administered to the upper third of the nasal cavity of a patient at risk for, or diagnosed with Huntington's disease. The effective amount of DFO is delivered directly to the patient's central nervous system for preconditioning, preventing and/or treating Huntingon's disease.

The invention discloses application of emricasan in the preparation of a medicine for treating ischemia/reperfusion injury. By using emricasan in treatment of ischemia/reperfusion injury, especially treatment of brain tissue neuropathy and even especially protective effect of cerebral ischemia/reperfusion (cerebral arterial thrombosis), cerebral ischemia/reperfusion injury can be remarkably mitigated.