57 results about "Hippocampal region" patented technology

A method of post-stroke treatment at delayed timepoints with sigma receptor agonists. Sigma receptors are promising targets for neuroprotection following ischemia. One of the key components in the demise of neurons following ischemic injury is the disruption of intracellular calcium homeostasis. The sigma receptor agonist, DTG, was shown to depress [Ca²⁺]_i elevations observed in response to ischemia induced by sodium azide and glucose deprivation. Two sigma receptor antagonists, metaphit and BD-1047, were shown to blunt the ability of DTG to inhibit ischemia-evoked increases in [Ca²⁺]_i. DTG inhibition of ischemia-induced increases in [Ca²⁺]_i was mimicked by the sigma-1 receptor-selective agonists, carbetapentane, (+)-pentazocine and PRE-084, but not by the sigma-2 selective agonist, ibogaine, showing that activation of sigma-1 receptors is responsible for the effects. Activation of sigma receptors can ameliorate [Ca²⁺]_i dysregulation associated with ischemia in cortical neurons, providing neuroprotective properties. The effects of 1,3-di-o-tolyguanidine (DTG), a high affinity sigma receptor agonist, as a potential treatment for decreasing infarct area at delayed time points was further examined in rats. DTG treatment significantly reduced infarct area in both cortical/striatal and cortical/hippocampal regions by >80%, relative to control rats. These findings were confirmed by immunohistochemical experiments using the neuronal marker, mouse anti-neuronal nuclei monoclonal antibody (NeuN), which showed that application of DTG significantly increased the number of viable neurons in these regions. Furthermore, DTG blocked the inflammatory response evoked by MCAO, as indicated by decreases in the number of reactive astrocytes and activated microglia/macrophages detected by immunostaining for glial fibrillary acidic protein (GFAP) and binding of isolectin IB4, respectively. Thus, the sigma receptor-selective agonist, DTG, can enhance neuronal survival when administered 24 hr after an ischemic stroke. In addition, the efficacy of sigma receptors for stroke treatment at delayed time points is likely the result of combined neuroprotective and anti-inflammatory properties of these receptors.

The invention provides a chemical heredity epilepsy persistent state disease animal model and a construction method and application thereof. The epilepsy persistent state disease animal model is a mouse brain kernel group (a hippocampus CA1 region and a thalamus anterior nucleus VA region of a model I); injecting a brain stereotaxic virus (a chemical genetic virus rAAV-CaMKIIa-hM3D (Gq)-mCherry-WPREs-pA) in an apricot kernel BLA region and a thalamus anterior nucleus VA region on the outer side of a substrate of the model II, and embedding an electrode array in a mouse hippocampus CA3 region;after the mouse is recovered for one week, a metabolite CNO of clozapine is injected into the abdominal cavity so that the CNO is combined with a virus expression receptor, neurons are activated to induce epileptic persistent state attack, and the epilepsy persistent state disease animal model is obtained through behavioral observation and in-vivo multichannel local field potential recording judgment. The epilepsy persistent state disease animal model constructed by the method is stable in seizure duration, high in success rate, low in death rate and good in repeatability, and has important significance in researching the origin and formation mechanism of epilepsy persistent state, and screening and mechanism of drug-resistant epilepsy persistent state drugs.

The invention discloses a method for constructing an Alzheimer disease mouse model. A genotype FVB-Fgf14Tg (tetO-MAPT* P301L) 4510 Kha/JlwsJ female mouse is adopted, a truncated tau protein or a vector expressing the truncated tau protein is injected into the brain of the mouse at the age of 4 months and then the mouse is fed for 2-4 months, and the amino acid sequence of the truncated tau proteinis as shown in SEQ ID NO: I. The Alzheimer disease mouse model is successfully constructed, tau pathology only appears in the hippocampus region of the constructed mouse model, and does not appear inother brain regions, the construction period is shortened to 6 months, and more than 50% of modeling time is saved.

The invention discloses application of cobra neurotoxin monomer molecules in treatment of senile dementia. The senile dementia, also known as Alzheimer disease, is a senile disease with progressive memory disorder, obstacle of judgment and reasoning ability as well as dyskinesia as main clinical features. Evidence shows that strong focal inflammatory responses exist in the brains of the patients with the senile dementia, and activated microglia and astrocytes exist near senile plaques; and the activated microglia and astrocytes can express a plurality of inflammatory cytokines, including interleukin-1[beta] (IL-1[beta]), tumor necrosisfactor-alpha (TNF-alpha) and the like. Therefore, experts suggest that neurodegeneration may be caused by inappropriate activation of immune and inflammatoryreactions in the brain; and super-strong immune reactions can attack nerve tissue "in the wrong direction", thereby causing neuron damage and death. In order to solve the problems, the invention discloses a group of cobra neurotoxin monomer molecules which can inhibit increase of contents of related inflammatory factors, namely the IL-1[beta]) and the TNF-alpha, in the hippocampus of rats with the senile dementia, as well as significantly shorten escape latency of the rats with the senile dementia after treatment in Morris water maze experiment.

The invention relates to a construction method of an AD model rat hippocampus difference gene expression chart by combining Abeta and D-gal. The construction method comprises the following steps: firstly, treating a rat with the Abeta and the D-gal to establish an AD model rat; secondly, measuring memory damage of the AD model rat by using a Morris water maze so as to determine successful construction of the AD model rat; thirdly, obtaining hippocampus samples of an AD model group and a normal control group, and respectively obtaining gene chip data of all tested hippocampus gene expressions;fourthly, uploading all the gene chip data to gene chip data analysis software, obtaining differential expression genes and screening a gene spectrum of the differential expressions of the AD model rat; fifthly, carrying out functional annotation classification and a biological pathway analysis on the differently-expressed genes to reveal molecular basis associated with the AD. According to the construction method disclosed by the invention, the Abeta and the D-gal are used as a whole AD model to study the gene expression spectrum of the AD model rat hippocampus genes, so that other errors changing the expressions and induced by exogenous genes are effectively avoided.

The invention provides application of tetrahedral framework nucleic acid in a medicine for treating epilepsy. The tetrahedral framework nucleic acid is formed by four single-stranded DNAs through base complementary pairing; the sequences of the four single-stranded DNAs are respectively selected from the sequences as shown in SEQ ID NO.1-4 in a one-to-one manner. The tetrahedral framework nucleic acid can inhibit down-regulation of glutamine synthetase in inflammatory glial cells by relieving proliferation of glial cells in a brain hippocampus and neuroinflammation caused by release of inflammatory factors, so that metabolism of excitatory glutamic acid is facilitated, and accumulation of glutamic acid and nervous excitability caused by accumulation of glutamic acid are relieved. Therefore, the tetrahedral framework nucleic acid can effectively control abnormal discharge of epilepsy and has potential clinical application prospects.

The invention relates to the technical field of biology, in particular to a method for improving social intercourse disorders of autism, and provides a method which can improve social intercourse disorders of an autism mouse model. According to the method, a specific knock-down vector specific to human-derived methyl CpG binding protein 2 (hMECP2) is constructed, and the specific knock-down vectoris injected into a hippocampal cornu ammonis 1 (CA1) region of the MECP2-transgene (MECP2-TG) autism mouse model by a stereotactic injection method, and thereby, the social intercourse disorders of the autism mouse model are improved.

The invention discloses an endogenous epileptic seizure animal model. The endogenous epileptic seizure animal model is constructed by adopting chemogenetics or optogenetics activation virus to be injected to a hippocampus CA3 region of a mouse and expressed for three weeks, wherein the activation virus is selected from: (a) a mixture of rAAV-CaMKIIa-hM3D(Gq)-mCherry-WPREs-pA and rAAV-VGAT1-hM3D(Gq)-mCherry-WPRE-pA, and (b) a mixture of rAAV-Ef1[alpha]-DIO-hChR2(H134R)-EYFP-WPRE-pA and rAAV-CaMKII-CRE-WPRE-pA as well as AAV-VGAT1-CRE-WPRE-pA. Compared with a CA1 region and VA region multi-point injection model, the epileptic seizure animal model is more suitable for mechanism research of epilepsy and screening of antiepileptic drugs.

The invention discloses a brain-like neural network with memory and information abstraction functions, the brain-like neural network uses working principles of a hippocampus region and a plurality of peripheral brain regions of a biological brain for reference, and the brain-like neural network comprises a memory module capable of forming scene memory, so that an intelligent agent can efficiently identify an object and carry out space navigation, reasoning and autonomous decision making. Features of each object can be quickly remembered, abstraction and meta-learning can be performed, generalization ability is high, lifelong learning can be performed, a synaptic plasticity process is adopted to adjust weights, partial differential operation is avoided, calculation overhead is lower than that of traditional deep learning, and a basis is provided for design and application of a neural mimicry chip.

The invention relates to a new application of ferroferric oxide nano-enzyme, which belongs to the field of western medicine pharmacy, and particularly relates to an application of polyethylene glycol-coated ferroferric oxide nano-enzyme (PEG-Fe3O4 nano-zyme) in promotion of neuroblastocyte proliferation and differentiation. After a small dose of PEG-Fe3O4 nanozyme is given to daily drinking water,the differentiation of neuroblasts in hippocampus can be increased, a blood-brain barrier is protected, autophagy is enhanced, and the oxygen free radical level is reduced. From the invention, the polyethylene glycol-coated ferroferric oxide nano-enzyme (PEG-Fe3O4 nano-enzyme) has the effect of promoting the differentiation of neuroblasts from multiple aspects, and has a certain value in the treatment of neurodegenerative diseases.

The invention relates to the technical field of neurotrophic factors (NTFs) and in particular relates to an application of acteoside to preparation of drugs for preventing nerve cell injuries caused by the NTFs and receptors thereof. Acteoside can obviously improve the expression of mRNA of NT-3, NGF and BDNF in brain tissues of female Kunming mice in model groups and the receptor TrkB of the BDNF, increase the protein content of the BDNF and TrkB in the brains and reinforce the protein expression levels of NT-3 and the NGF in the cortices and hippocampi of the brain tissues and the receptor TrkA of the NGF, indicating that acteoside has the function of reinforcing the NTFs and the receptors, can alleviate nerve cell injuries caused by reduction of expressions of the NTFs and the receptors thereof and has obviously better effects than vitamin E (VE) groups and piracetam tablet groups.

The invention belongs to the field of biological medicines, and particularly relates to application of probiotics in preparation of a medicine for treating progeny injury caused by pregnancy stress. The method comprises the following steps: carrying out stress on a pregnant mouse, simultaneously carrying out probiotic intervention, carrying out probiotic intervention until a child is adult after the child is born, and detecting the number of nick cells, the activation number of microglia cells, the expression level of apoptosis-related factors and the expression level of inflammatory factors of the adult child. Probiotic intervention is found to have a certain improvement effect on filial generation anxiety and cognitive impairment caused by pregnancy stress, activation of filial generation hippocampal microglial cells is reduced, damage and apoptosis of filial generation nerve cells are improved, meanwhile, inflammatory response in filial generation bodies is relieved, and the anti-stress effect of the filial generation is improved. Therefore, the probiotics can improve the pregnancy stress injury offspring and can be used for treating the injury of pregnancy stress on the offspring.

The invention relates to a brain-like relative navigation method based on social location cells/grid cells, and belongs to the field of cluster unmanned aerial vehicle intelligent navigation. According to the method, the relative positions of companions and the relative motor nervous mechanism of sensitive companions of a grid cell network are sensed by referring to a social position cell network of a hippocampal region of a bat. Firstly, a grid cell network model is constructed based on an attractor network to calculate endogenous relative position information between the unmanned aerial vehicles, and then a social contact position cell network model is constructed by using an isotropic Gaussian function to calculate exogenous relative position information between the unmanned aerial vehicles. Finally, the endogenous and exogenous relative position information are fused through a synaptic correlation learning algorithm to obtain relative position information between the unmanned aerial vehicles. The invention provides the brain-like relative navigation method which does not need linearization, is high in original signal fidelity, is learnable in architecture and is high in universality, and can be used for intelligent autonomous relative navigation of the cluster unmanned aerial vehicle in a satellite denial complex environment.

The invention belongs to the technical field of biomedicine, and particularly relates to an intracerebral endogenous neural stem cell magnetic resonance noninvasive tracing technology system and an establishment method. The spectrum characteristics of neural stem cells are analyzed in vitro to obtain the spectrum characteristics, the peak value of the spectrum characteristics can be used as a biological marker of the neural stem cells in vivo and vitro, after animal living body level verification, endogenous neural stem cells in a human brain are detected at the living body level, and the result shows that a small amount of neural stem cells exist in a hippocampus area, and the number of the neural stem cells is reduced along with age increase. According to the tracing technology system, the distribution and biological behaviors of endogenous neural stem cells in the brain can be traced in the living body level by using MRS (magnetic resonance spectroscopy), and the technology system provides a visual and noninvasive technical method for clinical neuroscience and clinical evaluation of nerve regeneration, regeneration indexes and the like in the brain, and has important clinical value and significance.

The invention relates to the technical field of gene engineering, in particular to a chimera for specifically degrading tau protein, an encoding gene of the chimera and application of the chimera andthe encoding gene. The chimera comprises a tau protein binding sequence, a connecting sequence and a ubiquitin ligase recruiting sequence, wherein the tau protein binding sequence is connected with the ubiquitin ligase recruiting sequence through the connecting sequence. The chimeric capable of specifically degrading the tau protein can enhance the degradation of the tau protein in cells, so thatthe content of the tau protein is reduced; a chimera in the AAV-PROTAC can be normally expressed in a hippocampal region of a C57BL/6 mouse, and human tau protein is effectively degraded; AAV-PROTAC is injected into the hippocampal region of a 3xTg AD model mouse, so that the human tau protein can be effectively degraded. Therefore, the chimera capable of specifically degrading the tau protein canplay a role in preventing and treating a series of tau diseases including Alzheimer's disease.

The invention discloses an electromagnetic radiation animal brain injury model construction method, and the method comprises the following steps: setting electromagnetic radiation conditions, and carrying out electromagnetic radiation treatment on a test animal; comparing the calcium activities of neurons in the hippocampus CA2 region of the experimental animal before and after the electromagnetic radiation treatment, and if the calcium activity variation has statistical significance, constructing the electromagnetic radiation animal brain injury model by using the electromagnetic radiation condition. According to the method, the electromagnetic radiation animal brain injury model can be well constructed, and possibility is increased for clarification of the molecular mechanism of the electromagnetic radiation brain injury effect and research and development of prevention and treatment drugs.

The invention relates to a bioactive composition for preventing and/or treating Alzheimer's disease and application thereof, and belongs to the technical field of biological medicine. The bioactive composition disclosed by the invention is prepared from the following components in parts by mass: 8 to 12 parts of melatonin, 190 to 210 parts of coenzyme Q10 and 55 to 65 parts of lecithin. The three components in the bioactive composition have a synergistic effect, and can play a role in protecting cells and organisms through different action mechanisms. The compatibility of the three components can significantly reduce the brain oxidative stress level of D-gal mice, reduce the tau protein phosphorylation level of the cerebral cortex and the hippocampus of the D-gal mice, reduce the brain aging degree and improve the learning and memory disorders of the mice compared with single use of a certain medicine, and provides a basis for prevention and/or treatment of the Alzheimer's disease. A new thought is provided for the development of medicines for preventing and/or treating the Alzheimer disease.

The invention discloses pitaya jelly and a preparation method. The pitaya jelly is prepared from the following components in parts by weight: 10-15 parts of pitaya juice, 3-5 parts of grape juice, 5-10 parts of jelly particles, 5-10 parts of raisins, 0.2-0.3 part of gellan gum, 0.2-0.3 part of carrageenan, 10-15 parts of sugar and 0.1-0.3 part of malic acid. 55 to 70 parts of distilled water; thejelly particles are prepared from crushed pitaya seeds, carrageenan, konjac glucomannan, sugar, malic acid and distilled water. According to the pitaya jelly and the preparation method thereof provided by the invention, during preparation, the pitaya seeds are ground into crushed pitaya seeds and are prepared into small-particle jelly particles, so that the surface fiber structure of the pitaya seeds is opened, the release of nutritional ingredients in the pitaya seeds is facilitated, and the absorption of arachidonic acid rich in the pitaya seeds by a human body is promoted, the jelly is beneficial to promoting neuroendocrine, accelerating growth of hippocampal neuronal cells, enhancing memory and prolonging the preservation time of arachidonic acid and other nutritional ingredients in pitaya, and nutrient substances are more effectively utilized.

The invention discloses a method for constructing an animal brain injury model based on hippocampal cholinergic neuron regulation, which comprises the following steps: setting electromagnetic radiation conditions, and carrying out electromagnetic radiation treatment on a test animal; and comparing the influence of cholinergic neuron activation or inhibition of the hippocampal CA3 region of the experimental animal on the behavior of the experimental animal before and after the electromagnetic radiation treatment, and if the influence on the behavior of the experimental animal has statistical significance, constructing the electromagnetic radiation animal brain injury model by utilizing the electromagnetic radiation condition. According to the method, the electromagnetic radiation animal brain injury model can be well constructed, and possibility is increased for clarification of the molecular mechanism of the electromagnetic radiation brain injury effect and research and development of prevention and treatment drugs.

The invention belongs to the technical field of functional marine product application, and discloses application of sciaenops ocellatus zymolyte in improving depression-like behaviors induced by chronic stress. A chronic stress depression model mouse is constructed, the sciaenops ocellatus zymolyte is subjected to intragastric administration, the effect of the sciaenops ocellatus zymolyte on improving system inflammation caused by chronic stress is investigated, and the result shows that after sciaenops ocellatus peptide intervention, the despair state time of the mouse is remarkably shortened, and the exploration desire of the mouse on an open space and a high-altitude environment is remarkably increased; the behavioral performance is recovered to a normal level, namely the depression-like behavior of the mouse is obviously improved. The intervention effect is better than that of a fish oil group; the preliminary research on the mechanism finds that the sciaenops ocellatus zymolyte has good improvement effects on the significant decrease of the chronic stress-induced hippocampal monoamine neurotransmitter level, the body system inflammation and the significant increase of the lipopolysaccharide level in serum; the research result provides a theoretical basis for developing the sciaenops ocellatus zymolyte into a new generation of green and safe anti-depression food.

The invention provides an RNAi adeno-associated virus for inhibiting Slc2a1 and a preparation method of the RNAi adeno-associated virus, wherein nucleic acid used by the RNAi is designed aiming at three interference sites on the Slc2a1. The adeno-associated virus disclosed by the invention can be used for remarkably and specifically inhibiting the expression of microglial cells Glut1; the mouse space learning and memory dysfunction caused by stress is obviously improved; the polarization of stress-induced microglial cells M1 can be inhibited, and the content of inflammatory factors in the hippocampus can be reduced; the compound is further applied to treatment of irritable learning and memory impairment, neuroinflammation and other diseases.

The invention relates to the technical field of plant extracts, in particular to application of a magnolia sieboldii extract in preparation of an anti-depression product. The magnolia sieboldii extract disclosed by the invention has an excellent anti-depression effect, and experimental results show that the magnolia sieboldii extract can effectively shorten the FTS immobility time and the TST immobility time of a depressive mouse; the number of hippocampal neurons in brain tissues of the mouse is increased; the expression quantity of the BDNF protein in the brain tissue is improved.

The invention belongs to the field of biological medicines and discloses application of formononetin in preparation of drugs for preventing and treating myocardial infarction combined with depression. The formononetin can obviously improve depression symptoms and myocardial dysfunction of mice suffering from myocardial infarction combined with depression. The formononetin can improve hypomotion, thought retardation, hypoactivity of willpower and inappetence, resist heart tissue apoptosis and/or resist brain tissue inflammation, can obviously increase expression of 5-HT and BDNF in the hippocampus, reduce expression of IL-6 and IL-17A in the hippocampus and serum, inhibit expression of in-vivo and in-vitro macrophage and microglial cell M1 type markers and promote expression of M2 type markers. The invention creatively provides application of formononetin in preparation of drugs for preventing and treating myocardial infarction combined with depression, interaction and side effects existing in drug combination are avoided, the probability of adverse reactions of patients is reduced, and a basis is provided for clinical practice of treating myocardial infarction combined with depression by formononetin.