18 results about "Neuronal apoptosis" patented technology

The invention discloses a neuronal apoptosis risk assessment system based on an oxidative stress signal axis. The neuronal apoptosis risk assessment system comprises the following steps: acquiring oxidative stress biomarker measurement data; calculating an oxidative stress signal axis activation index based on the oxidative stress biomarker measurement data; determining a neuronal apoptosis key factor expression level based on the oxidative stress signal axis activation index; calculating a neuronal apoptosis risk assessment value based on the neuronal apoptosis key factor expression level; and outputting the neuronal apoptosis risk assessment value. Compared with the prior art, the neuron apoptosis risk assessment method has the following advantages and effects: on the basis of integrated analysis of the oxidative stress signal axis multi-level biomarkers, through dynamic weight adjustment and activation index quantification, more accurate and systematic assessment of the neuron apoptosis risk is realized, and the reliability of risk assessment in non-diagnostic research is remarkably improved.

This invention discloses a wearable targeted static magnetic field device and its usage method for early intervention in Alzheimer's disease, belonging to the field of physical therapy equipment technology. The device consists of a permanent magnet array, a metal shield, a magnet support device, and a support shell suitable for wearing on the head. The device generates a constant static magnetic field spatial distribution with multiple focal points and a specific gradient within the wearer's skull through the arranged permanent magnet array. The characteristic parameters of this distribution include: multiple local intensity peaks of 10-50 mT and a spatial gradient of 0.5-5 T / m. As an intervention method, the static magnetic field can significantly inhibit Tau protein LLPS, reduce neuronal apoptosis, and improve the patient's cognitive function. This invention is a soft, elastic, wearable device that provides a novel, precisely targeted, and easy-to-use physical therapy solution for AD.

Disclosed in the present invention are a tricyclic compound, a preparation method therefor and the use thereof. The tricyclic compound of the present invention are a tricyclic compound as shown in I', a pharmaceutically acceptable salt thereof, a solvate thereof or a solvate of the pharmaceutically acceptable salt thereof. The tricyclic compound of the present invention is capable of protecting neurons, promoting repair of damaged neurons, inhibiting neuronal apoptosis, and slowing down AD cognitive decline, and have good pharmaceutical prospects.

Provided are molecules and compositions for eye-targeted gene therapy and methods of using the same. The eye-targeted gene therapy alleviates ischemic retinopathy by reducing pathologic neovascularization, gliosis and neuronal apoptosis.

The invention relates to the technical field of biological medicine and fundus disease treatment, in particular to application of Acbd3 in treatment of fundus diseases. In the retina of a fundus disease model mouse, the mRNA expression level and the protein expression level of Acbd3 are obviously increased relative to those of a control group. After the Acbd3 inhibitor is used, inflammatory response and neuronal apoptosis in the retina of the fundus disease model mouse are remarkably relieved, abnormal activation of Muller cells and microglial cells can be reduced, and the damaged blood-retina barrier can be repaired.

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.

This invention provides an oligosaccharide composition for improving neurodevelopment and functional disorders, comprising 6'-sialyl lactose and lactose-N-trisaccharide. The oligosaccharide composition provided by this invention can effectively inhibit the accumulation of Aβ protein, which leads to neuronal synaptic disorders, neuronal apoptosis, brain damage, and functional disorders. Therefore, the oligosaccharide composition provided by this invention can protect nerves and improve functional disorders. Furthermore, the oligosaccharide composition provided by this invention can also inhibit acetylcholinesterase activity, protect the normal development of cholinergic neurons, and increase neurotransmitter levels, thus benefiting the improvement of neurodevelopment, learning and memory abilities, and the improvement of behavioral coordination in infants and young children.

The invention discloses ascophyllum nodosum fucoidin ANFS, a preparation method thereof and application of the ascophyllum nodosum fucoidin ANFS in preparation of a preparation for preventing and treating Alzheimer's disease, and belongs to the technical field of marine biological medicine. The main chain of the ascophyllum nodosum fucoidin ANFS is composed of alpha-L fucoidin residues connected with (1-> 3), and the branch chain is monosaccharide or sulfate group. Sulfating modification occurs at C-2 and C-4 sites of fucose residues, and the molecular weight of the fucose residues is 15-30 kDa. Experiments prove that ANFS can remarkably improve the movement behavior defect of zebrafish, inhibit the activity of acetylcholin esterase, improve the activity of catalase and glutathione peroxidase, reduce the level of active oxygen in cells, reduce brain neuron apoptosis and effectively protect the integrity of a blood brain barrier. The polysaccharide is rich in source, simple and convenient in preparation process and high in safety, and has a wide application prospect in the aspect of developing marine drugs and functional products for treating the Alzheimer's disease.

The invention relates to an antibody drug for preventing and treating sepsis-related encephalopathy and application thereof. Variable region complementary determining regions and full-length amino acid sequences of a heavy chain and a light chain of an antibody are clear. The sepsis-related encephalopathy is high in morbidity and mortality, existing treatment means are limited, and the core pathogenesis of sepsis-related encephalopathy is related to blood-brain barrier injury and neuroinflammation. The A-FABP antibody 6H2 is combined with A-FABP through high affinity, the integrity of a blood brain barrier is protected, neuronal apoptosis is inhibited, symptoms of sepsis-related encephalopathy are remarkably improved, a breakthrough solution from symptomatic treatment to cause treatment is provided for the sepsis-related encephalopathy, and the A-FABP antibody 6H2 has important clinical application value.

The invention provides a co-assembly of a macrocyclic amphiphilic compound and an MST1 inhibitor as well as a preparation method and application of the co-assembly, and relates to the technical field of medicines. The co-assembly of the macrocyclic amphiphilic compound and the MST1 inhibitor is prepared from the macrocyclic amphiphilic compound, the MST1 inhibitor and Angiopep-2, wherein the macrocyclic amphiphilic compound and the MST1 inhibitor are co-assembled with the Angiopep-2; wherein the macrocyclic amphiphilic compound comprises a co-assembly body of guanidyl modified calixarene and cyclodextrin. According to the co-assembly disclosed by the invention, the treatment effect of the co-assembly on the Alzheimer's disease is enhanced by improving pathological processes such as neuronal apoptosis, neuroinflammation, synaptic plasticity injury and cognitive impairment in the Alzheimer's disease, and the limitation that only A beta is eliminated in the prior art is improved; according to the present invention, with the application of the polypeptide, the depolymerization and the removal of the A beta plaque, the fiber body and the oligomer can be achieved, the A beta cytotoxicity can be significantly reduced, the nerve cell apoptosis and the synaptic injury can be reduced, the cognitive disorder can be improved, and the comprehensive treatment effect can be provided.

The invention discloses an application of luteolin in preparation of a medicine for improving cognitive impairment induced by corticosterone (Cort), and relates to a medicine for improving cognitive impairment induced by corticosterone (Cort). By constructing a mouse cognitive impairment model induced by chronic Cort, research proves that the luteolin can remarkably improve the spatial learning and memory ability of a model mouse. The action mechanism is related to a multi-target synergistic effect, and mainly comprises the steps of relieving oxidative stress injury, inhibiting hippocampal neuron apoptosis, adjusting the autophagy level and enhancing synaptic plasticity. The new application and multi-mechanism synergistic effect of the luteolin for improving the Cort-induced cognitive impairment are defined, and a new technical scheme is provided for developing safe and effective cognitive impairment treatment medicines.

The invention discloses puerarin lipidosome with ginsenoside Rh2 as a lipid membrane material and a preparation method and application of the puerarin lipidosome, the membrane material cholesterol of the lipidosome is replaced with the lipidosome (Rh2-Pue-LP) of ginsenoside Rh2 de-entrapped puerarin, the Rh2-Pue-LP can inhibit and activate a JAK2-STAT3 signal channel, so that transcription of NLRP3 is inhibited, and the lipidosome has the advantages that the lipidosome can be used for preparing the puerarin lipidosome with the ginsenoside Rh2 as the lipid membrane material; the traditional Chinese medicine composition can be used for inhibiting microglial cell activation and neuronal apoptosis, effectively penetrating through a complete blood brain barrier (BBB), reaching a focus part and playing a role in neuroprotection.

This invention belongs to the field of pharmaceutical technology. Addressing the lack of reported applications of Astragalus injection in the preparation of drugs for treating cerebral hemorrhage, this invention proposes the use of Astragalus injection in the preparation of drugs for treating cerebral hemorrhage. Experimental results show that Astragalus injection can protect brain tissue neurons by inhibiting the HMGB1 / RAGE signaling pathway, inhibiting neuronal apoptosis, and reducing the expression of inflammatory factors in brain tissue, thereby achieving a protective effect against cerebral hemorrhage in rats. Therefore, Astragalus injection has the potential to be used as a drug for treating cerebral hemorrhage.

The invention discloses application of a transcription factor EGR1 in preparation of a medicine for treating traumatic brain injury, and relates to the technical field of medicines. By integrating transcriptomics and epigenomics analysis, the invention reveals the effect of EGR1 in regulating and controlling the mitochondrial homeostasis through an HIF1alpha / BNIP3 axis after trauma. EGR1 is found to be a key regulatory factor of TBI pathology, and the expression of EGR1 shows acute up-regulation in injured neurons. After the EGR1 gene is knocked out from a mouse, the neuron apoptosis is obviously reduced. Chromatin immunoprecipitation and dual luciferase reporter gene experiments show that EGR1 is directly combined with an HIF1alpha promoter to inhibit transcription of the HIF1alpha promoter. The deletion of EGR1 can enhance mitochondrial autophagy mediated by HIF1 alpha / BNIP3, so that mitochondrial dysfunction and oxidative stress in in-vitro and in-vivo experiments are reduced. On the contrary, the nerve protection effect of EGR1 knockout can be eliminated by silencing the HIF1alpha or the BNIP3. The discovery determines that an EGR1-HIF1 alpha-mitochondrial autophagy signal axis is used as an important determinant of TBI prognosis, and indicates that EGR1 has potential therapeutic value.

This invention provides the application of metformin in the preparation of a drug for treating learning and memory deficits caused by schizophrenia with normal glucose and lipid metabolism, belonging to the field of pharmaceutical technology. This invention discovers that metformin, under conditions of normal glucose and lipid metabolism, can effectively reduce neuronal apoptosis and neuroinflammatory damage in the prefrontal cortex of the brain in schizophrenia patients, thereby improving their learning and memory deficits. This invention further provides that the molecular target of metformin in repairing prefrontal cortex damage in schizophrenia is CTSS, and that it can downregulate the expression level of CTSS in the prefrontal cortex. The metformin described in this invention represents a repurposing of an existing drug, shortening drug development time and costs, and providing an effective drug treatment for learning and memory deficits caused by schizophrenia with normal glucose and lipid metabolism.

This invention relates to the field of probiotics technology, specifically to the application of a particular strain of *Lactobacillus paracasei* in the preparation of a strain for the prevention, relief, or treatment of cognitive impairment and related mood disorders caused by chronic sleep deprivation. The *Lactobacillus paracasei* is... Lactobacillus paracasei BKR005. This invention's probiotic indirectly promotes endogenous butyrate production by reshaping the gut microbiota, and effectively inhibits neuroinflammation and neuronal apoptosis through its unique MCT1 repair function, providing a clear target and novel mechanism for intervening in neuropsychiatric damage driven by chronic sleep deprivation.

The invention relates to a traditional Chinese medicine component compound. The traditional Chinese medicine component compound comprises baicalin, salidroside and catalpol. The traditional Chinese medicine component compound disclosed by the invention is a traditional Chinese medicine compound, pays attention to enhancement of an autoimmune system, and is free of toxic and side effects and reasonable in formula; the traditional Chinese medicine composition effectively aims at main pathogenesis of ischemic encephaledema and cerebral ischemia, such as reduction of cerebral moisture content, reduction of cerebral ischemia area, alleviation of neurological dysfunction, reduction of neuronal apoptosis and the like, and has a remarkable curative effect; the raw materials are wide in source and easy to obtain, can be extracted and biosynthesized by adopting crude drugs, can also be directly used as chemical synthesis products, and are convenient for preparation and large-scale production.

The invention provides application of a composition consisting of lily and rehmannia in preparation of a medicine for preventing and / or treating post-stroke depression, and particularly belongs to the technical field of traditional Chinese medicines. The invention discloses application of a composition consisting of lily and rehmannia in preparation of a medicine for preventing and / or treating post-stroke depression. The composition composed of the lily and the rehmannia has a treatment effect on post-stroke depression, the treatment effect is reflected in behavioral improvement, neuroprotection, nerve cell apoptosis inhibition, brain inflammation level reduction and neurotrophic pathway activation, and the ratio of the lily and rehmannia drug pairs is 1: 1, which is significantly better than the ratio of the lily and rehmannia drug pairs in 1: 0.5 and 1: 1.43.