38 results about "Neurotoxic effect" patented technology

Compositions and methods are disclosed in embodiments relating to induction of cell death such as in cancer cells. Compounds and related methods for synthesis and use thereof, including the use of compounds in therapy for the treatment of cancer and selective induction of apoptosis in cells are disclosed. Compounds are disclosed that have lower neurotoxicity effects than other compounds.

The invention relates to an application of ginsenoside Rg 1 for treating/preventing Alzheimer disease, and provides new use of ginsenoside Rg 1 in treating/preventing Alzheimer disease caused by A beta 1-42 induced neurotoxic effect. This provided Chinese medicinal monomer of ginsenoside Rg 1 has the following functions: protecting cytochondriome and reducing neuron apoptosis through relieving oligo-A beta 1-42 induced neuron stress injury, relieving inhibiting effect of A beta 1-42 on PKA-CREB signal passage, contributing to form long-term potentiation, and improving memory, thereby providing direct powerful experimental foundation and theoretical basis for ginsenoside Rg 1 in treating Alzheimer disease, and has high scientific and originality, and application value.

The present invention provides one kind of fusion protein in C-terminal of recombinant NMDA receptor NR2B subtype and produced through gene engineering process, polynucleotides encoding the fusion protein, and process of preparing and purifying the fusion protein. The fusion protein consists of the PSD95 linking region segment of NMDA receptor NR2B subtype and the transduction region segment of HIV coded Tat protein, and has one hemagglutinin marker segment for influenza virus inserted between the two above said segments. The fusion protein may be expressed effectively in colibacillus, has simple purifying process and is suitable for production in large scale. The Tat-HA-NR2B9C polypeptide of the present invention can block the interaction between NMDA receptor and PSD95, inhibit NMDA receptor mediated excitable neurotoxicity effect and protect nerves. It may be applied in treating cerebral apoplexy and relevant nerve diseases.

The present invention relates to the usage of wilfordii chlorine lactonic alcohol T4 for curing neural immune inflammatory diseases and provides a new usage of the wilfordii chlorine lactonic alcohol T4 for curing neural immune inflammatory diseases caused by the neural toxicity of microglia-mediated ABeta1-42 and LPS. The traditional medicine monomer of the wilfordii chlorine lactonic alcohol T4 has the following functions: obviously reducing the toxic damages of the oligmeric ABeta1-42 and LPS-induced gel-inflammation reaction on nerve cells, so as to protect the survival of nerve cells; inhibiting the level of inflammation medium produced by the oligmeric ABeta1-42 and the LPS-induced microglia cells; inhibiting the increase of iNOS and COX-2 expression of the oligmeric ABeta1-42 and the LPS-induced microglia cells; inhibiting the activation of NF-KappaB and JNK signal access of the oligmeric ABeta1-42 and the LPS-induced microglia cells. Therefore, the present invention provides direct powerful experimental evidence and theoretical basis for the application of the wilfordii chlorine lactonic alcohol T4 in neural immune inflammatory diseases, especially prevention and treatment of Alzheimer disease, thus having strong scientificity and creativity, as well as high development and application value.

The invention features methods for treating neurotoxicity associated with therapeutic agents, e.g., chemotherapeutic agents, and compositions and kits for use therein. The methods employ an extract of Ginkgo biloba to mitigate the neurotoxic effects of the therapeutic agents.

The invention provides compositions and methods for the induction of cell death, for example, cancer cell death. Combinations of compounds and related methods the use are disclosed, including the use of compounds in therapy for the treatment of cancer and selective induction of apoptosis in cells. The disclosed drug combinations can have lower neurotoxicity effects than other compounds and combinations of compounds.

The invention features methods for treating neurotoxicity associated with therapeutic agents, e.g., chemotherapeutic agents, and compositions and kits for use therein. The methods employ an extract of Ginkgo biloba to mitigate the neurotoxic effects of the therapeutic agents.

The invention provides a method for establishing an analysis module for assessing neurological functions. The method comprises the following steps: acquiring culture cells which include a plurality of fluorescent labels by virtue of a micro-fluorescent imaging system so as to conduct image analysis, wherein the culture cells include nerve cells and non-nerve cells; in accordance with area size of cell nucleuses and fluorescence intensity, selecting the nerve cells showing axon and dendrite fluorescent labels, eliminating non-nerve cells, and calculating the area sizes of the nerve cell bodies as well as axon and dendrite lengths and the number of branches, so that axon and dendrite growth situations of the nerve cells are determined; and in accordance with axon and dendrite fluorescent labeling ranges, calculating the number of synaptic puncta fluorescent labels on the nerve cells, so that the growth situation of the nerve cells is determined, and the neurological functions are assessed. The method disclosed by the invention can further serve as a drug screening platform, so as to rapidly detect whether drugs have a protective or neurotoxic effect on the nerve cells or not.

The invention discloses study on application of Muscone which is called as Mus for short in preparing a medicine for treating Alzheimer disease through modern biological technologies and bioinformatic analysis. The Mus is found to have an effect of restraining A beta neurovirulence and can reduce nerve cell death, so that the Muscone can be prepared into injection preparations for treating the Alzheimer disease to be used for treating the Alzheimer disease. The injection preparation for treating the Alzheimer disease is prepared by mixing Muscone compound 2%(v/v) ethyl alcohol and 98%(v/v) normal saline according to 500mu g to 1000mu l, and in-vivo intraperitoneal injection dose of the injection preparation is 2mg/Kg/day.

The invention relates to an application of tanshinone I shown in a formula I to the treatment of a microglia-mediated disease, in particular to an application of tanshinone I to the preparation of a medicament for treating and/or preventing the microglia-mediated disease, in particular to an application of tanshinone I to preparation of a medicament for treating and/or preventing psychoneuroimmunology chronic inflammatory diseases caused by microglia-mediated neurotoxic effects. The tanshinone I provided by the invention has the novel functions of remarkably suppressing microglia cell-activated and induced cell death, suppressing the generation and expression of inflammatory mediators, i.e., NO and TNF alpha of microglia cells, and remarkably lowering the cell toxicity of activated microglia cells on neurons, the tanshinone I can be applied to prevention and treatment of brain immune inflammation-related diseases such as Alzheimer's disease, Parkinson's disease, and the like. The formula I is shown in the specifications.

The invention relates to an application of fungus polyketide in preparation of a medicine used for treating alzheimer disease. According to the application, a fungus polyketide compound is prepared into an injection preparation used for treating the alzheimer disease, molecular weight of the fungus polyketide compound is 478.434Da, and 10mg/Kg injection preparation is intraperitoneally injected everytime; the fungus polyketide compound overcomes the defects that similar medicines in the past can not influence a pathological process and specificity can not be determined; a fungus polyketide compound injection medicine is adopted, is a small molecule compound, can penetrate through a blood brain barrier and can act on a pathological process of the alzheimer disease (AD), a decision for developing a medicine used for treating AD at present is met, an Abeta nerve toxic effect can be directly inhibited, and Abeta-induced nerve cell apoptosis is inhibited, namely nerve cell apoptosis is reduced by activating an Akt/GSK-3beta/beta-catenin signal channel.

The present invention discloses use of rhodiola root and spine date seed compound polysaccharide in preparation of anti neurodegenerative disease health food, the compound polysaccharide is a composition of rhodiola root polysaccharide and spine date seed polysaccharide, the compound polysaccharide is prepared from rhodiola root and /or spine date seed as raw materials by water extraction, concentration and alcohol precipitation process, the preparation method is simple, stable, efficient, and suitable for industrial production. By caenorhabditis elegans model experiment verification, the rhodiola root and spine date seed compound polysaccharide can effectively inhibit neurotoxicity of amyloid beta-protein and polyglutamine, the action mode is related with toxic protein aggregation inhibition, heat shock protein expression increase and reactive oxygen free radical level reduction, and neuroprotective effect can be shown.

The invention provides compositions and methods for the induction of cell death, for example, cancer cell death. Combinations of compounds and related methods of use are disclosed, including the use of compounds in therapy for the treatment of cancer and selective induction of apoptosis in cells. The disclosed drug combinations can have lower neurotoxicity effects than other compounds and combinations of compounds.

The present invention provides an improved process for the preparation of 1,2-Benzisoxazole-3-methanesulphonamide (Zonisamide), an anti-epileptic agent having anti-convulsant and anti-neurotoxic effects. In another aspect, the invention provides a key intermediate, 1,2-benzisoxazole-3-methane sodium sulfonate (BOS-Na:NaCl), isolated as a crystalline sodium chloride associated compound. The BOS-Na:NaCl isolated is directly converted to Zonisamide using a controlled molar ratio of chlorosulfonic acid to avoid conversion to the disulfonated side products.

The compositions of the invention are novel benzothiazol-based pyridinium compounds with potent acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inhibitory activities. Such compositions can be used, for example, to treat Alzheimer's Disease and other neurodegenerative disorders. The compounds of the invention can also be used to prevent or treat the neurotoxic effects of nerve agents (e.g., sarin gas or insecticides).

The invention relates to an application of D-seromycin in preparing medicine for treating Morphine psychological dependence behavior caused by stress, which belongs to the medicine technical field. A glutamic acid system in brain plays an important role in drug addiction process, and N-methyl-D-aspartic acid (NMDA) receptor which can be combined with glutamic acid to play a physiological effect exists in central nervous system. The NMDA receptor can be functionally inhibited by acting on different recognition sites. At present more side effects are brought by completely inhibiting the NMDA receptor, so antagonist which not only can block the pathological activation of the NMDA receptor but also is free from influencing the physiological activity of the NMDA receptor is important to discover. DCS is a serine natural derivative and is combined with a glycine site in NMDA receptor NR1 subunit to play an effect of excitant, so that internal flow of calcium ions in cells can be increased, but no neurotoxicity is produced. Since the prepared medicine not only can partially excite the NMDA receptor, but also is free from influencing the physiological activity, the medicine has small side effect on the human body.