8results about How to "Reduced infarct volume" patented technology

The application relates to the use of a TYK2 inhibitor, in particular a heterocyclic compound represented by the formula (I) or a pharmaceutically acceptable salt, solvate or isomer thereof in the preparation of a drug for treating or preventing ischemic stroke.

This invention relates to the field of biomedical technology, specifically disclosing a polypeptide and its application in the preparation of drugs for ischemic stroke. The amino acid sequence of the polypeptide is shown in SEQ ID NO. 1. This invention utilizes an in vivo tMCAO / R model and in vitro studies covering ischemic hypoxia (OGD) and neurotoxicity (MPP). + Multiple cell models of NL-PT, including those for cellular stress and hormonal stress (CORT), were used to reveal the application potential of the peptide NL-PT from multiple dimensions and levels. These results collectively demonstrate that NL-PT not only has a significant protective effect against the core pathological processes of ischemic stroke, but also exhibits broad-spectrum biological activity against various related injuries. In particular, its well-defined mechanism of anti-oxidative stress through scavenging reactive oxygen species (ROS) further highlights its multi-target intervention characteristics, providing solid and reliable experimental evidence for its development into a novel, multi-target therapeutic drug for ischemic stroke.

The application relates to the technical field of medicines, and particularly discloses a mitochondrion transfer promoter and application of the mitochondrion transfer promoter in preparation of medicines for preventing and treating post-CIRI mitochondrion dysfunction, wherein the active component of the promoter is decocted liquid of blue cloth and pyrola calliantha, and the mass ratio of the blue cloth to the pyrola calliantha is 2-4:1-2. The mitochondrion transfer promoter is prepared by decocting and extracting the blue cloth and the pyrola calliantha, animal experiments are conducted, it is found that the mitochondrion transfer promoter can significantly improve CIRI induced by cerebral middle artery ischemia-reperfusion, reduce a neurological function defect score, reduce a cerebral infarction volume, and it is proved by HE and Nissl staining that the mitochondrion transfer promoter can effectively improve neuron morphology and reduce neuron death. The mitochondrion transfer promoter can improve mitochondrion function, reduce oxidative stress, and enhance blood-brain barrier endothelial function, and has important clinical significance and practical value.

The invention discloses an application of white datura in preparation of a medicine for preventing and treating cerebral ischemia-reperfusion injury. The invention proposes and verifies that white datura can effectively prevent and treat ischemia reperfusion injury for the first time, including greatly reducing the volume of cerebral infarction caused by cerebral ischemia reperfusion; meanwhile, the neurological function impairment symptoms such as motor coordination and balance ability reduction, spatial learning and reference memory impairment and depression-like behaviors caused by cerebral ischemia reperfusion are remarkably improved, and a natural medicine with great application potential is provided for mechanism research, prevention and treatment of cerebral ischemia reperfusion injury.

The invention belongs to the technical field of ischemic stroke treatment, and discloses application of ULK1 possibly serving as a target spot for treating ischemic stroke. According to the invention, a photothrombotic stroke model is established, a ULK1 inhibitor SBI-0206965 (SBI), LYN1604 hydrochloride (LYN) and a ULK1 agonist are administered, and the ULK1 agonist is used for regulating the activity of ULK1 in vivo. Examples assess the outcome of sensory motor deficits, neuronal apoptosis, and microglia / macrophage activated neurological function. Immunofluorescence detection results show that ULK1 is mainly located in microglial cells in a post-ischemic infarction area of China. Upregulated ULK1 is treated by LYN, so that the infarct volume is remarkably reduced, the motor function is improved, and the increase of inflammatory microglial cells is promoted. In conclusion, the ULK1 promotes the repair of neurons and promotes the formation of 13 paths of anti-inflammatory microglial cell paths after ischemic injury.

The invention discloses an application of ginsenoside Ro in preparation of a medicine for treating cerebral ischemia-reperfusion injury. According to the application disclosed by the invention, by preparing a middle cerebral artery occlusion / reperfusion (MCAO) mouse model, the ginsenoside Ro is found to be capable of reducing the cerebral infarction volume of the model mouse, improving the pathological injury of brain tissues and increasing the cerebral blood flow at the ischemic side. Meanwhile, the ginsenoside Ro up-regulates the expression of brain tissue tight junction proteins ZO-1 and Occludin, inhibits the expression of matrix metalloproteinase MMP-9 / 2, reduces the leakage amount of Evans blue, and improves the blood brain barrier (BBB) dysfunction. Besides, by preparing an oxygen glucose deprivation / reperfusion (OGD / R) induced mouse brain microvascular endothelial cell line 3 (bEnd.3) cell model, it is found that the ginsenoside Ro can improve the damage of the barrier function of the bEnd.3 cell induced by the OGD / R, it is proved that the ginsenoside Ro can be used for the novel medical application of treating the cerebral arterial thrombosis, and the ginsenoside Ro has a wide application prospect.

The present application provides the use of aucubin or the combination of aucubin and ACA in the preparation of a medicament for treating ischemic brain injury, in particular acute cerebral ischemia-reperfusion injury. The present application first discovers that aucubin or the combination of aucubin and ACA can increase the blood flow of the ischemic side after ischemic brain injury in mice; significantly reduce the cerebral infarction volume; improve the cognitive and motor function of mice after ischemic brain injury; reduce the degree of injury caused by cerebral ischemia, significantly improve the degree of neuronal necrosis of brain tissue after ischemia; significantly increase the survival rate of HT22 cells after oxygen-glucose deprivation and reperfusion injury, reduce intracellular Ca 2+ fluorescence intensity, and inhibit cell apoptosis.

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.