12 results about "Stroke treatment" patented technology

The invention provides plasmin-targeted complement C3 derived anticoagulant polypeptide and application thereof, and belongs to the technical field of biological medicine. The present invention provides a complement C3-derived anticoagulant polypeptide (C3-HK10) and a modified peptide (C3-moHK10), which reduce nerve injury by enhancing the activity of plasmin in degrading fibrin thrombus and promoting the production of matBDNF (matured brain-derived neurotrophic factor), thereby protecting a host from dual threats of inflammatory thrombosis and neurological dysfunction, and also provides a method for preparing the anticoagulant polypeptide (C3-HK10) and a modified peptide (C3-moHK10). And good safety is shown. In conclusion, it is found for the first time that the complement C3 polypeptides C3-HK10 and C3-moHK10 have the characteristic of promoting plasmin activity, have the functions of inhibiting inflammation, thrombus and ischemic cerebral apoplexy injury and relieving nerve injury, and have the potential of becoming anti-inflammatory, thrombus and stroke treatment and neurological function drugs.

This invention discloses a brain-targeting neutrophil membrane-encapsulated tanshinone IIa PLGA nanoparticle formulation, its preparation method, and its uses. The brain-targeting tanshinone IIa nanoparticle formulation, Neu-Tan-IIa@PLGA, is characterized by comprising a PLGA-loaded tanshinone IIa nanoparticle core (Tan-IIa@PLGA) and an outer neutrophil membrane coating. This invention effectively overcomes the problems of poor water solubility, low oral bioavailability, and difficulty in crossing the blood-brain barrier associated with tanshinone IIa. This invention provides a tanshinone IIa with strong targeting and high drug stability, enabling delivery to lesions in ischemic brain regions and improving the safety and efficacy of stroke treatment.

Pharmaceutical compositions for treating an ischemic condition in a subject may include inhibitors of protein glycosylation. Methods may include administering to the subject in need thereof an effective amount an inhibitor of protein glycosylation. The administration may be effective to promote endothelial cell proliferation and angiogenesis in the subject. The subject may be in need of induced angiogenesis due to an ischemic condition caused by a stroke. Pharmaceutical compositions for inhibiting protein glycosylation in a cell may include ManN. Methods for inhibiting protein glycosylation in a cell may include administering to a cell an effective amount of ManN.

The application belongs to the technical field of heat stroke treatment, and specifically discloses application of DNAzyme in preparation of a medicine for treating heat stroke, wherein the DNAzyme is a DNAzyme for targeted regulation of ZBP1 protein expression. The application also discloses a medicine for preventing and treating heat stroke. The application has important value for fundamentally conquering the prevention and treatment method of heat stroke. The application fully verifies the remarkable efficacy of DNAzyme_SEQ_1 in the prevention and treatment of heat stroke through systematic experiments. The DNAzyme_SEQ_1 delivered by a TPNs carrier presents obvious liver and lung targeting in the mouse body, and the fluorescence intensity is obviously higher than that of other organs, thereby ensuring that the medicine precisely acts on the key damage sites of heat stroke.

The invention belongs to the field of stroke treatment, and provides an application of a metabolite Lacc-Phe or a synthetase CNDP2 thereof as an acute ischemic stroke treatment target, and a reagent for knocking out or knocking down the expression level of CNDP2 or an inhibitor of CNDP2 can be used for treating acute ischemic stroke or cerebral ischemia reperfusion injury. According to the application, an endogenous metabolite N-lactoyl phenylalanine (Lacc-Phe) and a synthetase CNDP2 thereof are found to be obviously increased after cerebral ischemia reperfusion injury, and the endogenous metabolite N-lactoyl phenylalanine (Lacc-Phe) and the synthetase CNDP2 thereof have relatively strong correlation with a reported cerebral arterial thrombosis marker; in addition, the knockout of the CNDP2 and the inhibitor bestatin (bestatin) of the CNDP2 can protect the cerebral ischemia reperfusion injury, and the overexpression of the CNDP2 and the exogenous administration of the Lacc-Phe can aggravate the cerebral ischemia reperfusion injury, so that the CNDP2 / Lacc-Phe axis can be used as a diagnosis, treatment and prognosis target of the cerebral arterial thrombosis disease.

The invention relates to a cerebral apoplexy treatment time window prolonging agent, application of the cerebral apoplexy treatment time window prolonging agent and a cerebral apoplexy thrombolysis kit, and the cerebral apoplexy treatment time window prolonging agent comprises a protein PAI-1 targeting inhibitor, the compound is used for being specifically combined with a plasminogen activator inhibitor PAI-1 released by activated platelets in a cerebral apoplexy thrombus area so as to inhibit the fibrinolytic inhibitory activity of the PAI-1. The invention has the beneficial effects that endogenous fibrinolysis is activated in a safe and effective way, the sharp contradiction between timeliness and safety in the prior art is directly solved, and the medicine is expected to be used as a safe early intervention medicine and provides new treatment possibility for a large number of patients who miss initial treatment opportunities. By means of the exquisite unlocking mechanism, the cerebral apoplexy treatment time window is delayed to 6 h, and precious time is gained for cerebral apoplexy treatment subsequently.

This invention provides a drug delivery system and its application based on brain microvascular endothelial cells, comprising stimulated brain microvascular endothelial cells, wherein the stimulation is performed by culturing in a culture system containing supernatant of brain microvascular endothelial cells cultured under glucose and oxygen deprivation. This invention solves the problems of targeting and timeliness in treating blood-brain barrier damage after ischemic stroke under current technologies. It can regulate the BBB while supporting its function and structure, maintaining and repairing BBB function after reperfusion, thus improving the prognosis of stroke treatment. The cell preparations in this invention are widely available and easily obtained, and can rapidly repair the blood-brain barrier. Furthermore, the cell preparations in this invention can target ischemic brain sites and can be administered via simple intravenous injection, facilitating clinical operation.

The application provides a construction method of an acute low-perfusion animal model and application thereof, and relates to the technical field of biomedicine. The construction method of the acute low-perfusion animal model of the application is aimed at brain capillary endothelial cells, and the animal model constructed is globally and durably low-perfused in brain microvessels, and the animal model has no infection or death risk and low cost. The animal model constructed by the application has important significance for researching the molecular mechanism of central nervous system injury caused by acute cerebral ischemia and developing a stroke treatment method.

The present application provides a temperature-sensitive hydrogel system for intranasal delivery of mesenchymal stem cells and application, which comprises a poloxamer hydrogel as a carrier and mesenchymal stem cells loaded on the carrier; the poloxamer hydrogel as a carrier comprises poloxamer 407 and poloxamer 188, and further comprises at least one of epidermal growth factor and fibroblast growth factor. The present application solves the problems of low efficiency of mesenchymal stem cells into the brain and poor survival ability of mesenchymal stem cells in the nasal cavity in the treatment of ischemic stroke under the current technology, improves the accumulation and activity of mesenchymal stem cells in the lesion site, and improves the prognosis of stroke treatment. The cell preparation in the present application can target the brain ischemic site, and can be administered by non-invasive intranasal administration, avoiding the risk of secondary trauma caused by invasive administration.

This invention belongs to the field of biomedical technology and discloses a methylene blue-fingolimod prodrug based on hypochlorous acid activation, its preparation method, and its application. Fingolimod and methylene blue, which has hypochlorous acid scavenging and neuroprotective functions, are bonded together via a hypochlorous acid-sensitive thioether bridge. This design cleverly utilizes the abnormally high concentration of hypochlorous acid within the lesion as "molecular scissors," achieving precise activation of the prodrug at the target site and synergistic release of both drugs. This not only endows fingolimod with targeted noise reduction and enhanced efficacy but also simultaneously implements a combined attack of "detoxification" and "anti-inflammation," thereby more thoroughly breaking the damage cascade and providing a novel synergistic solution for stroke treatment.