18 results about "Neuron apoptosis" patented technology

The application relates to the technical field of biological medicine and fundus disease treatment, in particular to application of Acbd3 in treatment of fundus diseases. It is found that the mRNA expression level and the protein expression level of Acbd3 in the retina of a fundus disease model mouse are significantly higher than those of a control group. After an Acbd3 inhibitor is used, the inflammatory reaction and neuron apoptosis in the retina of the fundus disease model mouse are significantly relieved, abnormal activation of Muller cells and microglia cells can be reduced, and a damaged blood-retina barrier can be repaired.

The application discloses application of TESC as an Alzheimer's disease prevention and treatment target and relates to the field of biological medicines. A TESC overexpression (TESC-OE) hippocampal neuron cell line is constructed through lentivirus transfection, and the result shows that TESC-OE has the ability to resist A beta-induced neuron apoptosis and synapse damage. A TESC overexpression model in the hippocampus of a mouse is constructed through stereotactic injection of an adeno-associated virus, and the result shows that the hippocampal gray matter volume in the brain of the TESC-OE mouse is significantly larger than that of a wild type mouse. A beta stereotactic modeling is performed on the basis of TESC overexpression in the hippocampus, and the result shows that the TESC-OE mouse can significantly resist A beta-induced hippocampal atrophy, learning and memory dysfunction and impaired synaptic plasticity. Immunoblotting analysis reveals the molecular mechanism that TESC can increase the expression of anti-apoptotic genes in the hippocampus and reduce the expression of pro-apoptotic genes to exert a neuroprotective effect.

The invention discloses a composite microneedle with bacterial outer membrane vesicles loaded with active ingredients as well as a preparation method and application of the composite microneedle. The composite microneedle is prepared from the bacterial outer membrane vesicles and the active ingredients loaded in the bacterial outer membrane vesicles, the bacterial outer membrane vesicles are derived from mucus eubacterium, the active ingredient is cycloastragenol, and the composite microneedle has a transdermal delivery function and delivers the active ingredient to a target tissue in a targeted manner. The method comprises the following steps: firstly, encapsulating cycloastragenol into mucus eubacterium outer membrane vesicles through a co-incubation or active drug loading technology to form a composite nano-carrier; the EL-OMVs-CAG compound prepared by the invention has good biocompatibility and blood brain barrier penetrating ability, and can target a central nervous system, regulate the activity of microglial cells, inhibit neuroinflammatory response and reduce synaptic loss and neuronal apoptosis in a hippocampal region, so that cognitive function impairment caused by operation and anesthesia is improved.

The invention discloses a TREM1 specific antagonistic peptide based on AI de novo design and application thereof, and belongs to the technical field of biological medicine. The novel antagonistic peptide Pep457 is finally obtained by taking an immunoglobulin-like structural domain of TREM1 protein as a target spot, performing de novo design by utilizing an RFdiffusion model and combining molecular docking and binding free energy calculation, and detecting and evaluating the in-vitro inhibitory activity of the novel antagonistic peptide Pep457, and the amino acid sequence of the novel antagonistic peptide Pep457 is shown as SEQ ID NO: 1. In a traumatic brain injury mouse model, the Pep457 can remarkably relieve blood brain barrier damage, relieve encephaledema, inhibit neuroinflammation and neuronal apoptosis and effectively promote movement and cognitive function recovery. The invention provides a novel efficient candidate drug for treating TREM1 related inflammatory diseases, especially traumatic nerve injury, and has an important clinical application prospect.

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.

The application relates to the field of medical health, and discloses a nerve protection method and system based on AMPK-Pak2 channel regulation, which comprises the following steps: establishing a channel-damage relationship graph by using the AMPK activity level, the Pak2 function state and the nerve function score of a nerve injury patient; matching AMPK-Pak2 targeted drugs of the nerve injury patient according to AMPK-Pak2 channel regulation abnormality typing, and positioning the nerve injury area to set the AMPK-Pak2 channel regulation mode of the nerve injury patient; calculating the nerve protection efficiency index of the nerve injury patient to generate an adaptive adjustment instruction of the AMPK-Pak2 channel regulation mode; identifying the treatment response state of the nerve injury patient by using the neuron apoptosis rate and the nerve function score; and outputting a treatment execution scheme of the nerve injury patient based on the treatment response state and in combination with the AMPK-Pak2 channel regulation mode and the adaptive adjustment instruction. The application can target the regulation of key signal channels in cells and improve the overall recovery effect of nerve function.

The application belongs to the technical field of biological medicine, and particularly relates to a short peptide for blocking the combination of VDBP and Megalin. The application directly reveals the core molecular basis of the combination of VDBP and Megalin by identifying the key amino acid site sequence of the interaction between VDBP and Megalin. The blocking small molecules or polypeptides designed on the basis can cut off the combination of VDBP and Megalin in a highly specific manner, avoiding the limitations brought by random screening and large molecule antibody intervention in the traditional method. The technical scheme not only significantly improves the research and development efficiency, reduces redundant experiments, and reduces the research and development cost, but also guarantees the repeatability and consistency of the research results. Based on the combination site, the application directly designs a short peptide capable of blocking the combination of VDBP and Megalin, the short peptide does not cause neuron apoptosis or structural damage, can reverse the inhibited signal pathway of the interaction between VDBP and Megalin, and has potential application value in treating depression.

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 is applicable to the technical field of biological medicines, and provides application of lisinopril in preparation of a medicine for treating amyotrophic lateral sclerosis. The invention has important value for promoting research and development of amyotrophic lateral sclerosis (ALS) treatment medicines and improving prognosis of patients. In-vitro experiments show that lisinopril can prevent mitochondria damage of NSC34 cells induced by SOD1G93A, expression of Beclin 1, LC3 and p62 is regulated by inhibiting a TGF [beta] 1 / PI3K / AKT / mTOR signal channel, cell autophagy is activated, and neuronal apoptosis is inhibited. In-vivo experiments show that lisinopril can activate in-vivo BI1 expression, regulate ALS model mouse lipid content and intervene in a glycerophospholipid metabolic process, and also can inhibit motor neuron death, myelin sheath shedding and neuromuscular junction degeneration and promote mitochondrial biogenesis by influencing autophagy regulated by a TGF [beta] 1 / PI3K / AKT / mTOR pathway.

The application discloses a method for evaluating the influence of heat stress on the neurotoxicity of Eriocheir sinensis and application thereof, wherein the neurotoxicity refers to neuron heat damage toxicity caused by heat stress, the neuron apoptosis, DNA damage, neuron cell damage biomarker (NSE) and heat shock response of Eriocheir sinensis are used as judgment parameters of the neurotoxicity, and the above features are comprehensively analyzed to evaluate the heat damage toxicity of heat stress on the nerve tissue of Eriocheir sinensis. The evaluation method has high reliability, operability and practicability, provides a new method for accurately detecting and evaluating the neurotoxicity of Eriocheir sinensis, and provides help for screening Eriocheir sinensis fry groups with high high-temperature adaptability, high high-temperature tolerance and high survival ability.

The application discloses application of Alvelestat in preparation of a medicine for treating cerebral hemorrhage. The application is based on proteomic stratification analysis of hematoma fluid of a cerebral hemorrhage patient, finds that neutrophil elastase (NE) is a key molecule in the progression of cerebral hemorrhage, and further proposes a technical scheme of taking NE as a target and using a selective NE inhibitor Alvelestat for intervention. Animal experiments verify that Alvelestat can reduce cerebral edema, promote hematoma absorption, reduce neuron apoptosis and improve neural function defects; transcriptomics reveals that it plays a protective role by inhibiting multiple inflammation and immunity related signal pathways. The application provides a new strategy for precise targeted treatment of cerebral hemorrhage, and has clear clinical conversion value.

The invention discloses application of a separated USP18 gene in preparation of a medicine for treating and / or preventing Parkinson's disease, and belongs to the technical field of crossing of genetic engineering and biological pharmacy. And the nucleotide sequence of the USP18 gene is shown as SEQ ID NO. 3 or SEQ ID NO. 7. The invention provides a recombinant vector containing the gene. Through specific overexpression of USP18 in an in-vitro cell experiment and an in-vivo animal experiment, a synergistic treatment effect is generated: in an MPP + induced cell model, c-Caspase3 can be remarkably inhibited, the ratio of Bax / Bcl-2 is reduced, and neuronal apoptosis is effectively resisted; in a Parkinson's disease mouse model, loss of TH positive dopaminergic neurons in a nigra region can be specifically rescued, and the movement function in open field, pole climbing and bar rotating experiments is comprehensively improved. A brand new efficient target spot and a treatment scheme are provided for gene therapy of Parkinson's disease.

The invention belongs to the technical field of biological medicines, and particularly relates to an oligopeptide for blocking combination of VDBP and Megalin. By clearly identifying a key amino acid site sequence of interaction of VDBP and Megalin, a core molecular basis of combination of VDBP and Megalin is directly disclosed. The blocking micromolecule or polypeptide designed on the basis can cut off the combination of the blocking micromolecule or polypeptide and the blocking micromolecule or polypeptide in a high-specificity mode, and limitation caused by random screening and macromolecular antibody intervention in a traditional method is avoided. According to the technical scheme, the research and development efficiency is remarkably improved, redundant experiments are reduced, the research and development cost is reduced, and the repeatability and consistency of research results are guaranteed. Based on the binding site, the invention directly designs a short peptide capable of blocking binding of VDBP and Megalin, the short peptide does not cause neuronal apoptosis or structural damage, can reverse a signal channel inhibited by interaction of VDBP and Megalin, and has potential application value in treatment of depression.

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 application discloses a TREM1 specific antagonistic peptide based on AI de novo design and application thereof, and belongs to the technical field of biological medicine. The immunoglobulin-like domain of the TREM1 protein is taken as a target point, and a RFdiffusion model is used for de novo design, and multi-stage screening is carried out in combination with molecular docking and calculation of binding free energy, in vitro inhibitory activity is detected and evaluated, and finally a novel antagonistic peptide Pep457 is obtained, and the amino acid sequence of the novel antagonistic peptide Pep457 is shown as SEQ ID NO:1. In a mouse model of traumatic brain injury, Pep457 can significantly reduce blood-brain barrier damage, relieve brain edema, inhibit neuroinflammation and neuron apoptosis, and effectively promote the recovery of motor and cognitive functions. The application provides a new high-efficiency candidate drug for the treatment of TREM1 related inflammatory diseases, especially traumatic nerve injury, and has an important clinical application prospect.

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.

The invention discloses application of a snakegourd peel injection in preparation of a medicine for treating spinal cord injury, and relates to the technical field of biological medicines. SCI mouse model research finds that TPI can promote motor function recovery after SCI, relieve tissue damage, protect neuron structures, inhibit neuroinflammation, promote polarization of microglial cells to anti-inflammatory phenotypes, relieve oxidative stress after spinal cord injury, inhibit neuronal apoptosis and promote axonal regeneration, and can be used for preparing the medicine for treating the spinal cord injury. The potential action mechanism of the TPI is disclosed through network pharmacology and molecular docking, and the high consistency of an in-vivo experiment result and an in-vitro prediction result enhances the rationality of taking the TPI or an active component thereof as a candidate drug for SCI treatment.