56 results about "Autoimmune encephalomyelitis" patented technology

A medicine for treatment of multiple sclerosis comprising, as an effective component, ibudilast represented by the chemical formula (1) below. Ibudilast is effective to experimental autoimmune encephalomyelitis by oral administration, and is effective to multiple sclerosis which is a disease of a central nervous system.

The present invention provides an isolated antibody that binds a fibrin or fibrinogen γC domain. In various aspects, the antibody inhibits microglial adhesion to the fibrin or fibrinogen γC domain, inhibits Mac-1 binding to the fibrin or fibrinogen γC domain, and/or suppresses clinical symptoms of Experimental Autoimmune Encephalomyelitis (EAE). Various methods of using the antibodies, pharmaceutical compositions, kits, vectors, cells comprising the vectors, and antibody generating methods are provided.

Neurotrophin binding to its specific receptors Trk A and p75 leads to the activation of multiple signalling cascades, culminating in neuroprotective and regenerative effects, including neuronal survival and neurite outgrowth. Neurotrophic factors have been used for the treatment of several neurodegenerative diseases. However, their use is limited by their inability to cross the blood-brain barrier, their short half life and their side effects. Small molecule neurotrophin mimetics may be beneficial in treating a number of neurodegenerative disorders. The present invention shows the capacity of nerve growth factor agonist molecules of Formulae I-IV, as defined in the specification, to induce differentiation in PC 12 cells, promote survival in RN22 cells and activate Trk A, IkBa and SAPK/JNK phosphorylation to various extents in both cell lines. In addition these molecules were able to ameliorate acute experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS) animal model, inhibiting brain inflammation and reducing brain damage. We also observed suppression in the production of pro-inflammatory genes like the inducible nitric oxide synthase. These small molecules with NGF agonist activity may be beneficial for MS and other neurodegenerative diseases due to its neuroprotective and immunomodulatory properties.

The invention discloses applications of vorinostat in aspect of drugs for treating autoimmune diseases. The experiment result disclosed by the invention shows that due to the vorinostat, the morbidity of the experimental autoimmune encephalomyelitis of mice is reudced, and also the average score, the highest score and the total score of clinical marks are reduced; spinal cord inflammatory cell infiltration and spinal cord demyelination can be alleviated; the weight percent of a cell Th1 related to IFN (Interferon)-gamma secretion and a cell Th17 cell related to IL-17A secretion accounting for positive T cells CD4 in the spleen can be reduced. Therefore the invention relates to the preparation of the drug for inhibiting the experimental autoimmune encephalomyelitis of an animal model, and the drug is expected to treat the diseases related to multiple sclerosis, ophthalmoneuromyelitis, acute disseminated encephalomyelitis and the like.

The invention provides application of magnolol to preparation of a drug for preventing and/or treating myelitis. The magnolol can significantly reduce inflammatory cell infiltration in EAE model mouse spinal cord, and also significantly alleviates demyelination phenomenon. Therefore, the magnolol can be used for preparing the drug for preventing or treating autoimmune encephalomyelitis. The invention provides a novel therapeutic drug for clinical treatment of autoimmune encephalomyelitis.

The invention discloses application of chrysin in preparation of medicaments for treating autoimmune diseases. Experimental results show that the chrysin can inhibit differentiation of human immune dendritic cells (DC) and maturity of LPS (lipopolysaccharide)-activated human immune DC, can inhibit the antigen uptake capabilities of the immature DC and the antigen presenting capabilities of the mature DC and can inhibit T cell proliferation reactions stimulated by the DC. In particular, the chrysin can reduce the average score, the highest score and the total score of clinical scores of experimental autoimmune encephalomyelitis of mice and can relieve myelitis cell infiltration and demyelination in spinal cords. Thus, the medicament inhibiting immune systems is expected to become the medicament for treating such autoimmune inflammatory diseases as multiple sclerosis, neuromyelitis optica and acute disseminated encephalomyelitis clinically.

The present invention is based on the finding that inhibition of eotaxin-2 by polyclonal or monoclonal antibodies, has a significant protective effect in animal models of inflammatory diseases such as rheumatoid arthritis, experimental autoimmune encephalomyelitis (EAE), colitis, diabetes, and atherosclerosis. The invention thus provides pharmaceutical compositions comprising specific anti-eotaxin 2 antibodies for use alone or in combination with other therapeutic agents in the treatment of inflammatory, autoimmune and cardiovascular diseases. The invention also provides specific anti-eotaxin-2 monoclonal antibodies, and methods of treatment utilizing the antibodies of the invention.

The invention discloses an intervention effect of a ginsenoside Rg1 on autoimmune encephalomyelitis mouse, belonging to the field of Chinese herbal medicine monomer intervening disease. The autoimmune encephalomyelitis (EAE) model of cord sheath oligodendrocyte glycoprotein peptide MOG35-55 immune C57BL / 6 mouse is an international accepted multiple sclerosis mouse animal model, establishing the model, and simultaneously inducing, using the ginsenoside Rg1 to intervene, through observing the impact of the ginsenoside Rg1 on the phenotype and the histopathology of the EAE model, obtaining that the ginsenoside Rg1 can significantly reduce the incidence of the autoimmune encephalomyelitis. Therefore, the ginsenoside Rg1 has a certain role in the intervention of multiple sclerosis. The ginsenoside Rg1 can significantly reduce the disease incidence of the multiple sclerosis animal model-EAE mice.

The invention discloses a method for establishing a Macaca fascicularis experimental autoimmune encephalomyelitis model and application thereof. According to a concrete technical scheme in the invention, the method comprises the following steps: preparing an emulsion (an MOG solution: CFA = 1: 1) from MOG 34-56 (100 mu g/ml); narcotizing Macaca fascicularis for experiments and injecting 1 ml of the prepared emulsion at 10 injection points; carrying out immunization injection of the emulsion (secondary immunization) according to the above-mentioned method and dose in 7 days after the primary immunization injection (primary immunization); carrying out clinical observation in one day after primary immunization and recording clinical scores; and determining pathogenic sites, degrees and the like by using an MRI iconographic method at pathogenic time nodes. The model established in the invention has an application value which cannot be achieved by other rodent models, has the characteristics of recurrence-alleviation type attacks, low cost, wide availability of Macaca fascicularis for experiments and the like compared with a Macaca rhesus model and has a wide application scope in fields related to multiple sclerosis diseases.

The proliferation and activation of microglia is emerging as an important etiologic factor and target for therapeutic intervention in several CNS diseases, including Alzheimer's disease and multiple sclerosis. Here, we have discovered that retinoic acids dramatically inhibit microglial proliferation in an in vivo model including the widely-used animal model of multiple sclerosis, the experimental autoimmune encephalomyelitis (EAE) mouse model.

Preparation and application of line leaf inula flower lactone A in the multiple sclerosis, having a structure of

Line leaf inula flower lactone A has therapeutic effects on experimental autoimmune encephalomyelitis (EAE) model, and is used to develop drug for treating multiple sclerosis (MS). Line leaf inula flower lactone A drug is a combination containing the active ingredient of line leaf inula flower lactone A and conventional pharmaceutically carrier, and may be in forms of tablets, dispersible tablets, mouth collapse tablets, retard tablets, capsule, soft capsule, dropping pill, granules, injection, powder injection, or aerosol. The pharmaceutical composition is used for treating multiple sclerosis, has tremendous developing potentiality because of its high value of clinical application.

The invention provides a modification method and application of an in-vitro immunocyte preparation. The method comprises the following steps: preparing an EAE (Experimental Autoimmune Encephalomyelitis) model by utilizing a MOG-35-55 peptide fragment in an immunizing manner; inducing encephalitogenic immunocyte: after immunizing, co-culturing spleen T cells and spleen macrophages, and Fasudil for 72 hours at the 9 day, so as to obtain the encephalitogenic immunocyte: Fasudil modified T cells and Fasudil modified macrophages. A treatment effect on an EAE mouse by Fasudil modified immunocyte is observed and a result proves that the Fasudil in-vitro modified immunocyte can be used for effectively alleviating clinical symptoms of the EAE mouse; the treatment effect of the Fasudil modified macrophages is better than that of the Fasudil modified T cells. Furthermore, the Fasudil in-vitro modified immunocyte also has the advantages of small side effect, low treatment cost and the like, and has good clinical application prospect on the treatment of neurodegenerative diseases.

The invention discloses application of carnosol in preparation of medicines for preventing and treating experimental autoimmune encephalomyelitis. Whole animal model experiments verifies that the carnosol not only can effectively delay the occurrence and development of the experimental autoimmune encephalomyelitis, significantly reduces the infiltration of peripheral inflammatory cells into the central nervous system and relieves the degree of demyelination, but also can promote the transformation of infiltrating macrophages and intrinsic microglial proinflammatory phenotypes to an M2 phenotype with an immunoregulatory function. Furthermore, the carnosol can inhibite Th17 cell differentiation and STAT3 phosphorylation and block NF-kappa B nuclear translocation of a transcription factor. Therefore, the carnosol has a great potential in the preparation of the medicines for preventing and treating the autoimmune diseases such as multiple sclerosis.

The present application relates to extracts from Rehmannia glutinosa as a therapeutic agent for multiple sclerosis. The present application also relates to the use of a digitalis extract, verbascoside, or a combination of catalpol, verbascoside, motherwoside, and digitoxin D in the manufacture of a medicament for preventing or treating multiple sclerosis in a patient. The present invention also relates to the use of radix rehmanniae extract, verbascoside, or a combination consisting of catalpol, verbascoside, motherwoside, and digitoxin D in the preparation of a medicament for preventing or treating experimental autoimmune encephalomyelitis in a patient.

As described herein, lactosylceramide (LacCer) levels are up-regulated in the CNS during chronic experimental autoimmune encephalomyelitis (EAE), an experimental model of multiple sclerosis (MS). LacCer acts in an autocrine manner to trigger transcriptional programs that promote the recruitment and activation of CNS infiltrating monocytes and microglia, and neurodegeneration. In addition, increased B4GALT6 expression and LacCer levels were detected in CNS MS lesions in human patients. Finally, the inhibition of LacCer synthesis suppressed local CNS innate immunity and neurodegeneration in EAE, and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 is a therapeutic target for MS and other neuroinflammatory disorders.

The invention discloses application of 2-(2-difluoromethyl benzimidazole-1-yl)-4,6-dimorpholinyl-1,3,5-triazine (ZSTK474 for short) to preparation of a medicine for treating autoimmune and inflammatory diseases. Experimental results prove that the ZSTK474 can inhibit the differentiation of human immune dendritic cells, the maturity of the lipopolysaccharide (LPS) activated human immune dendritic cells, the antigen uptake capacity of immature dendritic cells, the antigen presenting capacity of mature dendritic cells and T cell proliferation reaction stimulated by the dendritic cells, and particularly can reduce the morbidity degree of mouse experimental autoimmune encephalomyelitis, so the ZSTK474 is expected to become a medicine for treating autoimmune and inflammatory diseases such as multiple sclerosis, acute disseminated encephalomyelitis and the like clinically.

The invention discloses application of ellagic acid to preparation of a medicine for preventing and treating multiple sclerosis. An experimental autoimmune encephalomyelitis whole animal model experiment proves that the occurrence and development of experimental autoimmune encephalomyelitis can be effectively prevented through oral administration or intraperitoneal injection of the ellagic acid; the infiltration of peripheral inflammatory cells to a central nervous system is remarkably inhibited and the demyelination degree is alleviated; the ellagic acid also has a very good treatment effecton model animals at an initial period and fastigium of incidence. Therefore, the ellagic acid has a great potential for preparing the medicine for preventing and treating the multiple sclerosis.

The invention discloses application of a fused immune protein to preparation of medicine for treating multiple sclerosis and belongs to the field of biological engineering. The fused immune protein has specific effect of relieving chronic EVE (experimental autoimmune encephalomyelitis) mouse clinical impairment. In a treatment course, hormone-like drug withdrawal rebound phenomenon does not appear. The fused immune protein can be used for preparing the medicine for treating multiple sclerosis independently or can be used for preparing the medicine for treating multiple sclerosis with other medicines.

The invention belongs to the technical field of biological medicines, and relates to an application of ellagic acid and a metabolic derivative urolithin compound thereof in preparation of medicines for treating autoimmune diseases and immunological rejection after organ/tissue transplantation. The invention takes classic animal models related to autoimmunity and immunoregulation, namely experimental autoimmune encephalomyelitis, ulcerative colitis and skin transplantation as examples. The multi-angle experiments in multiple aspects such as nerve function score, lesion tissue pathology change, inflammatory factor expression, pro-inflammatory cell number and the like prove that the ellagic acid and the metabolic derivative thereof remarkably relieve the degree of experimental autoimmune encephalomyelitis disease and inhibit infiltration of inflammatory cells to the center; the pathological state of ulcerative colitis is obviously improved, and the colon length is recovered; the inflammatory cell infiltration of the skin graft in a skin transplantation model can be inhibited, the regulatory T cell proportion can be up-regulated, the immune tolerance can be enhanced, and the clinical application value and the development prospect are relatively high.

The invention relates to a new medicinal application of Huperzine A, specifically the application in preparation of medicines preventing and treating multiple sclerosis disease, falling into the pharmaceutical field. Huperzine A is a Chinese medicine effective component monomer with the structure of formula (I). The present invention uses whole animal model experiments, and the results show that Huperzine A has significant improvement on the neurological function score of a mouse model with experimental autoimmune encephalomyelitis, and obvious inhibition effect on inflammatory cell infiltration of the central nervous system, and can be used in preparing medicines preventing and treating multiple sclerosis disease.

Experimental autoimmune encephalomyelitis (EAE) is a ThI-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). Herein it is demonstrated that CXCR2, a chemokine receptor involved in the recruitment of neutrophils, is expressed in tissues with EAE lesions. Blockade or deficiency of CXCR2 reduces the infiltration of neutrophils to sites of inflammation. Thus provided herein are reagents that antagonize or inhibit ELR+CXC chemokines and methods of use of these reagents in preventing and treating organ-specific autoimmune diseases like multiple sclerosis, and methods or treating various inflammatory conditions and diseases.

The invention provides a method of producing human immature dental pulp stem cells (hIDPSCs) expressing CD44 and CD13 and lacking expression of CD146. The invention also provides compositions for use in the treatment of a neurological disease or condition selected from the group consisting of Parkinson's disease (PD), multiple sclerosis, amyotrophic lateral sclerosis (ALS), stroke, autoimmune encephalomyelitis, diabetic neuropathy, glaucomatous neuropathy, Alzheimer's disease, Huntington's disease (HD), autism, schizophrenia, stroke, ischemia, a motor disorder, and a convulsive disorder.