70 results about "Middle cerebral artery occlusion" patented technology

The invention discloses HGG (Human Gammaglobulin) polypeptide in combination with the tissue specificity of cerebral arterial thrombosis. The invention relates to a method for obtaining the polypeptide. The method comprises the following steps: carrying out in-vivo selection of a mouse MCAO (Middle Cerebral Artery Occlusion) cerebral arterial thrombosis model by adopting an in-vivo phage display peptide library screening technology so as to obtain phage clones in combination with cerebral arterial thrombosis tissue; and randomly selecting the plurality of phage clones to sequence, and authenticating the in-vivo combination specificity of HGG peptide and coded phage clones HGG-M13 thereof. The invention further relates to application of the polypeptide in preparation of a high-sensitivity imaging molecular probe and a targeting delivery neuroprotective drug for cerebral stroke. The polypeptide can be synthesized through an artificial method; the polypeptide is low in molecular weight, high in activity and penetrating power, good in specificity and low in toxicity, and has good tissue targeting of cerebral arterial thrombosis in vivo; and therefore, the polypeptide is applicable to serving as a carrier of the high-sensitivity imaging molecular probe and the targeting delivery neuroprotective drug.

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 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 the technical field of drugs and aims to provide a new use of nafamostat mesilate in preparing drugs for preventing and curing ischemic cerebral apoplexy. Preoperative preventative administration or postoperative therapeutic administration is performed on a classical permanent cerebral ischemia model (permanent middle cerebral artery occlusion-pMCAO) and a classical cerebral ischemia reperfusion model (transient middle cerebral artery occlusion-tMCAO) by the invention, respectively, and the results show that the nafamostat mesilate is remarkable in effect of resisting the ischemic cerebral apoplexy. At a dosage point appointed by experiments, the nafamostat mesilate can be used for obviously improving animal behavior dysfunctions caused by ischemia and lowering the cerebral infarction rate of permanent cerebral ischemia and cerebral ischemia reperfusion rats. Prompted by research results, the nafamostat mesilate can be used for preventing and curing the ischemic cerebral apoplexy.

The invention relates to application of tanshinone IIA derivative in the preparation of ischemic stroke drugs and belongs to the field of medicine. The high-molecular tanshinone IIA derivative is synthesized herein; pharmacological experiment studies on animals are carried out; experimental results show that the high-molecular tanshinone IIA derivative can well protect cerebral ischemia-reperfusion injury in MCAO (middle cerebral artery occlusion) animal model of an SD (Sprague Dawley) rat; compared with positive controls, the high-molecular tanshinone IIA derivative can evidently improve neurological behaviors, cerebral infarction area and encephaledema of the rat with focal cerebral ischemia. The high-molecular tanshinone IIA derivative provided by the invention helps provide a new ideafor treating ischemic stroke, and has the potential of being developed into drugs to treat ischemic stroke.

The invention belongs to the field of pharmacy and relates to a new application of a traditional Chinese medicine motherwort extract in pharmacy, in particular to the application of the purified motherwort extract in preparing nerve protection medicine for treating cerebral injury, especially the application of the purified motherwort extract in preparing brain protection medicine for treating artery obstruction in the brain. By an animal experiment of the purified motherwort extract, a result indicates that the brain stem volume is obviously reduced after the purified motherwort extract is applied, the obstacle grading of the nerve function is decreased by being compared with a contrast group, the total antioxidant concentration in plasma is increased, the DNA oxidation injury is reduced, the expression levels of apoptosis and apoptosis promoting protein are reduced, and the content of apoptosis resistance protein is also increased. The purified motherwort extract can be used for preparing the nerve protection medicine for treating the cerebral injury and can effectively treat cerebral apoplexy.

The invention discloses an amide compound for treating stroke and a preparation method thereof. A structural formula of the amide compound is shown as follows, wherein R1-R3 independently represent hydrogen or fluorine, R4 represents hydrogen or hydroxyl, R5 represents C1-C20 alkyl or C2-C20 alkenyl, n is an integer from 0 to 4, and respectively independent configuration representation of*1-*4 is R or S. The amide compound is synthesized through esterification reaction and ammonolysis reaction and is simple to operate and high in yield and purity. The amide compound has effects of thrombolysis and promoting recovery of brain tissue and nerve function, has obvious recovery effect on ischemic brain injury and nerve injury caused by a middle cerebral artery occlusion induced by a suture-occluded method, does not present toxic and side effect and can be used as a drug for treating stroke.

The invention discloses a method for making a guinea pig MCAO (middle cerebral artery occlusion) model, which comprises the steps of preparing an anesthetic, weighing a guinea pig, and injecting a certain amount of the anesthetic into the abdominal cavity according to the weight of the guinea pig, so that the guinea pig is anesthetized; placing the guinea pig on a temperature control blanket, fixing the guinea pig on an operating table with the body of the guinea pig straight and free of tension, scraping the neck hair of the guinea pig with a hair clipper, and locally sterilizing with entoiodine; cutting the skin along the paracervical median of the guinea pig to open the anterior cervical fascia and expose the sternocleidomastoid muscle on the right side, then separating the anterior cervical muscle group and sternocleidomastoid muscle, and drawing with a fine silk thread to separate the muscle tissues until a complete CCA (common carotid artery) is observed. Compared with the traditional common carotid artery plug-in method, the method has the advantages that blood is directly supplied from the common carotid artery through the internal carotid artery after reperfusion, the common carotid artery is directly ligated after reperfusion, the reperfusion blood supply can only be circulated through lateral branches, the reperfusion effect similar to the clinical effect can be achieved, and the success rate of model preparation is high.

The invention discloses new medicinal application of senkyunolide I shown in a structural formula (I). In the application, the influence of the senkyunolide I on the cerebral blood flow change of rats in a reperfusion model of local cerebral ischemia caused by middle cerebral artery occlusion (MCAO) of the rats and a kalium chloratum (KCL) induced rat cortical spreading depression model is studied by adopting an animal model, and pharmacological results prove that the senkyunolide I can improve the cerebral blood flow of the rats after MCAO molding obviously and can restore and exceed the original cerebral blood flow formed before modeling quickly after reperfusion so as to play a certain role in cerebral protection. In addition, the senkyunolide I can resist the condition that cerebral blood flow descends due to KCL-induced rat local cerebral vasoconstriction, so the senkyunolide I can be used for preparing medicaments for the prevention and treatment of cerebral apoplexy and relevant treatment during convalescence.

The invention discloses application of epicannabidiol hydrate in preparing drugs for preventing and/or curing brain injuries and a pharmaceutical composition comprising the epicannabidiol hydrate. According to the application of the epicannabidiol hydrate in preparing the drugs for preventing and/or curing the brain injuries, it is the first time to discover that the epicannabidiol hydrate has a drug effect of obviously relieving a brain injury caused by a cerebral ischemic stroke. Researches show that the epicannabidiol hydrate relieves in vitro and vivo neural inflammatory reactions by inhibiting expression of a proinflammatory factor and promoting expression of an anti-inflammatory factor, has a function of obviously decreasing the volume of cerebral infarction after transient middle cerebral artery occlusion, relieves inflammatory overreactions of ischemic brain tissue, and realizes a neuroprotective effect after cerebral ischemia, and can be effectively applied to preventing and/or curing the brain injuries, especially the brain injury caused by the cerebral ischemic stroke; and the pharmaceutical composition comprising the epicannabidiol hydrate can become a novel drug for preventing and/or curing the brain injuries of brain diseases closely associated with brain inflammations, and various brain diseases can be cured.

The invention provides an application of a flavonoid glycoside compound on a medicine for treating cerebral apoplexy. A compound with a structure represented by a formula I is apigenin-7-O-beta-D-(6''-p-coumaroyl)-glucopy ranoside. The pharmacological test results prove that the compound has an obvious protection effect on ischemic injury caused by a middle cerebral artery occlusion (MACO) model and is free from toxic and side effects. The application of the flavonoid glycoside compound on the medicine for treating the cerebral apoplexy provided by the invention can provide a lead compound for preparing new medicines for protecting cerebral ischemic injury, so that the flavonoid glycoside compound can be a new medicine for treating the cerebral apoplexy.

The invention belongs to the technical field of medicine and pharmacology, and discloses a drug for treating cerebral apoplexy and a construction method of an endogenous stem cell expression animal model, and the drug for treating cerebral apoplexy is liver-softening collateral-dredging decoction. The number of rat brain tissue BrdU, BrdU/NeuN and BrdU/GFAP positive cells in each group at each time point is detected through an ischemia reperfusion model caused by middle cerebral artery occlusion, and the influence of the liver softening and collateral dredging soup on proliferation and differentiation of endogenous neural stem cells of rats with ischemic brain injury is analyzed. According to the method, an improved Longa method is adopted to manufacture an ischemia-reperfusion brain injury model caused by MCAO type middle cerebral artery occlusion of rats; it is verified that the liver-softening collateral-dredging decoction promotes proliferation of endogenous neural stem cells of ischemia-reperfusion brain injury rats, differentiates the endogenous neural stem cells into mature neurons, inhibits excessive proliferation of astrocytes, promotes nerve regeneration and repair and improves nerve functions.

The invention belongs to the field of pharmaceuticals and relates to application of totarol serving as a natural product extracted from podocarpus totara to preparation of a drug for preventing and treating ischemic cerebral apoplexy. A result obtained by researching glutamic acid of rat cortex neurons, a hypoxia and hypoglycemia model and a rat middle cerebral artery occlusion experimental model shows that the totarol can be used for reducing neurotoxicity caused by glutamic acid, reducing neuron injury caused by hypoxia and hypoglycemia, improving the activity of glutathione peroxidase in cortical neurons and brain tissues and the activity of superoxide dismutase, reducing the volume of cerebral ischemia infarct caused after cerebral apoplexy and improving the scores of neurological behaviors. The result proves that the totarol has a remarkable neuroprotective effect for ischemic brain tissues and can be used for preparing a drug for preventing and treating ischemic cerebral apoplexy.

The invention provides a pharmaceutical composite for treating cerebral stroke, which is prepared from the following ingredients in portion by weight: 1-50 portions of astragalosides, 1-50 portions of salvia miltiorrhiza extract and 0.5-30 portions of ligusticum chuanxiong oil. The invention further provides a medicine prepared from the active pharmaceutical ingredients of astragalosides, salvia miltiorrhiza extract and ligusticum chuanxiong oil. The medicine, due to the adoption of middle cerebral artery occlusion model (MCAO model) and the application of modern histopathology, flow cytometry and molecular biotechnology, has the effect of reducing cerebral infarction volume, protecting nerve cell, inhibiting apoptosis after cerebral ischaemia and blocking inflammatory reaction in ischemic infarction area. Through experiment, the result shows that, due to the compatibility of three ingredients, the medicine has the advantages of obvious synergism, definite efficacy and controllable quality, thereby clinically providing a new medicine for treating cerebral stroke.

The invention discloses new medicinal application of senkyunolide J shown in a structural formula (I). In the application, the influence of the senkyunolide J on the cerebral blood flow change of rats in a reperfusion model of local cerebral ischemia caused by middle cerebral artery occlusion (MCAO) of the rats and a kalium chloratum (KCL) induced rat cortical spreading depression model is studied by adopting an animal model, and pharmacological results prove that the senkyunolide J can improve the cerebral blood flow of the rats after MCAO molding obviously and can restore and exceed the original cerebral blood flow formed before modeling quickly after reperfusion so as to play a certain role in cerebral protection. In addition, the senkyunolide J can resist the condition that cerebral blood flow descends due to KCL-induced rat local cerebral vasoconstriction, so the senkyunolide J can be used for preparing medicaments for resisting cerebral apoplexy.

The invention provides a trocar applied to middle cerebral artery occlusion models, and belongs to the field of medical apparatus and instruments. The trocar can be recycled and comprises a puncture needle, a core and a suture. The puncture needle comprises a needle, a fixing wing and a fixing connector, the fixing wing is fixed to a side surface of the needle, the tapered top of the fixing connector is connected with the bottom of the needle, and a tapered opening is formed in the bottom of the fixing connector; the core comprises a core body and a fixing interface, and the taper of the tapered top of the fixing interface is identical to the taper of the opening in the bottom of the fixing connector, so that the fixing interface can assuredly cling to the fixing connector; the core is used for fixing the integral trocar, and effects of stopping bleeding and preventing the puncture needle from penetrating blood vessels can be realized; the suture is of a commercially available structure. The trocar has the advantages that the puncture needle is used for being arranged in the blood vessels, the core can be pushed into the puncture needle, the puncture needle can be prevented from piecing the blood vessels, and the suture can be inserted into the core and can penetrate the core to reach target blood vessel locations; the trocar is simple in structure and low in manufacturing cost, and can be conveniently and quickly operated, the puncture needle can be arranged in the blood vessels and can be simultaneously fixed, and accordingly bleeding can be stopped by means of blocking.

The invention relates to application of a medicine taking alpha-asarone as a unique pharmacological active component in treatment of cerebral arterial thrombosis. The medicine provided by the invention can be used for effectively treating cerebral arterial thrombosis and has no obvious toxic or side effect. The medicine can obviously increase the blood flow ratio of the infarct side half brain to the opposite side half brain of a middle cerebral artery occlusion ischemia reperfusion rat and reduce the cerebral infarction volume; the nerve function score is obviously improved, and the lifetime of the model rat is prolonged; the occurrence rate of epilepsy caused by cerebral arterial thrombosis is obviously reduced.

The invention discloses application of medioresinol in preparation of a drug for preventing or treating the cerebral injury and a pharmaceutical composition thereof. The invention provides applicationof medioresinol in preparation of a drug for preventing or treating the cerebral injury for the first time; the medioresinol has an obvious effect on prevention or treatment of the cerebral injury, especially the cerebral injury caused by the cerebral arterial thrombosis; and the cerebral injury caused by the cerebral arterial thrombosis can be obviously reduced. The experiment discovers that themedioresinol has an effect of inhibiting brain microvascular endothelial cell damage caused by oxygen-glucose deprivation and is capable of obviously reducing the permeability of a blood brain barrier under oxygen-glucose deprivation. The medioresinol can reduce the volume of cerebral infarction under middle cerebral artery occlusion remarkably. The pharmaceutical composition containing the medioresinol can become a novel drug for preventing and/or treating the cerebral injury and is used for treating various cerebrovascular diseases including cerebral arterial thrombosis.

Small molecule agonists, partial agonists, and antagonists for the TrkA receptor are described. The compounds are gambogic amines, where the carboxylic acid group of gambogic acid (CO₂H) has been replaced by an amine group (CH₂NR₁R₂). In some embodiments, the compounds selectively bind to TrkA but not TrkB or C, robustly induce its tyrosine phosphorylation and downstream signaling activation including Akt and MAP kinases. Further, they can strongly prevent glutamate-induced neuronal cell death and provoke prominent neurite outgrowth in PC12 cells. Gambogic amines specifically interact with the cytoplasmic juxtamembrane domain of TrkA receptor and trigger its dimerization. Administration of these compounds in can substantially diminishes Kainic acid-triggered neuronal cell death and decrease infarct volume in transient middle cerebral artery occlusion (MCAO) model of stroke. Thus, these compounds can provide effective treatments for debilitating neurodegenerative diseases and provide neuroprotection from patients suffering from stroke or other ischemic events.