35 results about "Glial scar" patented technology

The invention relates to a fibroin three-dimensional bracket for nervus centralis remediation, and belongs to the field of biological medicinal materials. The fibroin three-dimensional bracket comprises fibroin protein fiber with grooves, fibroin protein/hyaluronic acid plural gel and fibroin membrane conduits. By adopting the fibroin three-dimensional bracket, defects that a conventional bracket is low in mechanical property, low in biodegradability and the like are overcome. By adopting the fibroin three-dimensional bracket, physiological states of an extracellular matrix can be simulated, adhesion, migration, amplification and differentiation of cells can be facilitated, and furthermore orientated growth of axon to fracture parts can be guided; due to connection of the bracket, glial scars can be inhibited, and thus remediation of a nervus centralis system can be facilitated; and the bracket can be applied to basic research on neural injury remediation, can be also applied to bridging remediation of human body spinal cord injury or deficiency, and has good biomedical prospects.

It is an object of the present invention to provide a novel neuronal regeneration promoting agent, particularly a neuronal regeneration promoting agent having an inhibitory effect on glial scar formation. The present invention provides a neuronal regeneration promoting agent which comprises an inhibitor of a bone morphogenetic protein type 1A receptor (BMPR1A) as an active ingredient.

The invention relates to the field of machines, in particular to a precision mouse spinal cord clamping injury clamp and clamping injury force adjusting method. The distance between the abutting side of the clamp and the clamping penetrating side of the clamp is adjusted by screwing in or screwing out an abutting screw so as to adjust the clamping force. The method comprises the following steps of selecting a female mouse with the weight ranging from 18 g to 21 g, precisely positioning the eleventh vertebral body of the mouse, conducting an osteotomy on the back vertebral plate of the vertebral body, and clamping the segment of the spinal cord to be injured in the left-right direction with a special improved vascular clamp, so that molding is successful. Compared with the prior art, the method for building the spinal cord injury model is simple and easy to implement, precise, easy to repeat, high in success rate and the like. After an injury, behavior indicators, spinal cord injury pathological indicators and glial scar indicators are observed, the method can well simulate the real process formed after the human spinal cord injury, the simulation degree is quite high, the real process is highly reproduced, and the method has the advantages beyond comparison with existing methods.

The present invention relates to a method of treating disorders of the nervous system and more particularly disorders associated with a gliotic response and/or an inflammatory response within the central nervous system and to therapeutic agents useful for same. More particularly, the present invention involves a method of preventing or reducing the amount of Eph receptor-mediated gliosis and/or glial scarring and/or inflammation and/or Eph receptor-mediated inhibition of axonal growth which occurs during and/or after disease or injury to the nervous system. The present invention also facilitates the identification of therapeutic agents which modulate Eph receptor-mediated signaling. The method and therapeutic agents of the present invention are useful for treating a range of nervous system diseases, conditions and injuries including, inter alia, paralysis induced by physiological-, pathological- or trauma-induced injury to the brain or spinal cord.

The invention belongs to the field of medicine preparation, and particularly relates to application of Adjudin in preparing medicine for inhibiting glial scar formation. The glial scar is formed by activation and proliferation of astrocyte after central lesion. The medicine is at least in a form of tablets, capsules, granules, dripping pills, suspensions, syrup, enteric-coated preparation, emulsion suspension and injections. Experiments show that Adjudin can effectively reduce size of the glial scar of mice after brain tissue injury; in an in-vitro primary cell scratch model, Adjudin remarkably inhibits proliferation and migration of astrocyte cells, improves ethology of the mice after brain injury and promotes recovery, so that Adjudin has important application value in preparing the medicine for inhibiting glial scar formation.

The invention belongs to the technical field of cytobiology and provides an establishment method of an in-vitro glial scar forming model. The establishment method of the in-vitro glial scar forming model comprises the steps that purified meninx (meningo) fiber cells and purified astroglia cells are planted in adjacent small cells on a cavity glass slide respectively with a certain amount ratio, and a culture medium is added for culture; after the cells grow in an adherent mode, a partition board between the small cells is removed, and culture continues to be conducted; when it is observed that the meninx (meningo) fiber cells and the astroglia cells grow and come close to each other, mechanical scratching is conducted at the junction of the two kinds of cells so as to damage the cells, and finally, a glial scar structure is formed. The in-vitro glial scar forming model obtained through the method can well simulate the whole forming process of an in-vitro glial scar, the corresponding glial scar form structure and the change relevant to the cytobiology and the molecular biology appear, and an in-vitro cell-level experimental model is provided for studying of the glial scar forming mechanism and relevant treatment.

The invention provides a method utilizing a surface microstructure to activate neural astrocyte, and belongs to the technical field of cell culture. The method comprises the following steps: (1) obtaining a PDMS cell culture surface with an uneven microstructure; (2) adopting primarily cultured neurogliocyte as the activation object, and after the cells grow to the phase of cell fusion, digesting cells by pancreatin (0.25%) to prepare cell suspension; (3) adding the cell suspension to the microstructure surface, and after cell attachment, culturing the cells for 1 to 14 days; (4) identifying the neural astrocyte obtained by the method mentioned above to find a series of activation expressions that cells carry out EMT conversion, cell stem property is enhanced, and glucose transportation is strengthened. The method has the advantage that a physical microstructure on the surface of a culture medium is utilized to activate neural astrocyte and at the same time, formation of glial scar caused by reactive hyperplasia of colloid cells can be avoided. The provided method has a wide application prospect in the treatment of destructive disease and degenerative disease of nervous system.

The invention provides in-situ injectable hydrogel for treating central nervous injury and a preparation method of the in-situ injectable hydrogel. The hydrogel is formed by performing click chemical coupling on X-Y through functional groups on arginine-glycine-aspartic acid modified multi-arm polyethylene glycol-X and multi-arm polyethylene glycol-Y, nano/micron particles and growth factors of slow-release immunoregulation and/or antioxidant drugs loaded on the hydrogel through chemical coupling reaction are coated in the hydrogel. The injection hydrogel disclosed by the invention can be used for precisely and slowly releasing the immunomodulatory and/or antioxidant drug and the growth factor locally at an injured part, so that the formation of a cystic cavity after spinal cord injury is prevented, secondary injury caused by neuroinflammation is relieved, residual spinal cord nervous tissues and axons are protected, and the formation of glial scar tissues is reduced; a penetrable extracellular matrix environment is provided for regeneration of body nerve axons, further recovery of electrophysiology and motor functions is promoted, and the method can be used for repairing injury of soft tissues such as spinal cords and the like.

According to the invention, human induced pluripotent stem cells are differentiated into NSCs in vitro, human umbilical cords are separated and cultured into MSC auxiliary materials, the materials are used according to the proportion of 1: 1, PBS is used as a solvent, an obtained cell biological product is jointly transplanted to the spinal cord of a mouse with acute spinal cord injury (at the thoracic marrow T10 stage) in situ, nerve injury repair is effectively promoted, and the motor function is improved. The product for treating animal acute spinal cord injury can be differentiated into neurons and glial cells in the host body, reduce the glial scar area, reduce fibrosis and reduce the inflammation level, so that the animal motor function, especially limb coordination, is improved, and the product fully plays a role in subsequent treatment of the spinal cord injury and promotion of tissue repair.

The present invention relates to a method of inducing neuronal production in a subject, a method of recruiting neurons to a subject's brain, and a method of treating a neurodegenerative condition by administering a neurotrophic factor and an inhibitor of pro-gliogenic bone morphogenetic proteins. Also disclosed is a method of suppressing astrocyte generation and inducing neuronal production in a subject, a method of treating a neurologic condition, and a method of suppressing glial scar formation in a subject by administering an inhibitor of pro-gliogenic bone morphogenetic proteins. Finally, the present invention involves a method of introducing a heterogeneous protein into a subject's brain and spinal cord by introducing a nucleic acid molecule encoding the heterogeneous protein introduced into the subject's ependyma, permitting the protein from the nucleic acid molecule to be expressed within the subject's ependyma, and permitting the expressed protein to migrate within the subject's brain and spinal cord.

The invention discloses a Western medicine compound for treatment of spinal cord injury and a use thereof. The Western medicine compound is composed of gabexate mesylate and nitrofurantoin, wherein the mass ratio of gabexate mesilate to nitrofurantoin is (0.09-0.13) to 1. When the Western medicine compound is applied to the treatment of spinal cord injury, the adult injection dosage of the Western medicine compound is 1.9-2.1 mg/kg, and the drug administration is performed 6-12 h later after spinal cord injury. Through test treatment of a spinal cord injury modeling animal, the Western medicine compound is found out to reduce cell apoptosis, promote nerve cell survival, inhibit formation of glial scar and significantly improve BBB scores of the animal after treatment, and the Western medicine compound is indicated to have a significant effect on promoting motion function recovery after spinal cord injury. Compared with a commonly used drug methylprednisolone for treating spinal cord injury in clinic at current, the Western medicine compound has the advantages of wider drug administration window, more lasting treatment effect and better long-term effect.

The invention discloses a western medicine composition for treating spinal cord injury, and an application of the composition. The western medicine composition consists of hexoprenaline and sulbactam, wherein a mass ratio of hexoprenaline to sulbactam is (0.17-0.22) : 1; and when the western medicine composition is used for treating the spinal cord injury, an injection dose for adults is 0.95-1.00mg/kg, and the administration time is 6-24 hours after the spinal cord injury. Through test treatment of a model of an animal with spinal cord injury, it is discovered that the western medicine composition can reduce cell apoptosis, facilitate neuronal survival, inhibit glial scar formation and remarkably improve a BBB score of the treated animal, so that the western medicine composition has a remarkable promotion effect for motor function recovery after the spinal cord injury. Compared with an existing common medicine-methylprednisolone used for treating the spinal cord injury in clinic, the western medicine composition has the advantages that an administration window is wider, the treatment effect is more lasting, and the long-term effect is better.

A method includes applying salmon fibrin at a central nervous system injury site. For example, applying salmon fibrin can include injecting salmon fibrin. The method can also include causing the suppression of astrocyte activation, whereby glial scarring is at least reduced. The functional recovery of a patient who has suffered a central nervous system injury is promoted according to this method.

The invention discloses a western medicine compound for treating fracture. The western medicine compound consists of ulinastatin and levofloxacin, wherein the mass ratio of the ulinastatin to the levofloxacin is 0.09-0.13: 1; when the western medicine compound is used for treating the fracture, the injected dose of the western medicine compound for adults is 1.9-2.1 mg/kg, and the drug administration time is the time of 6-12 hours after fracture. Through testing therapy to fracture molding animals, the western medicine compound can reduce cell apoptosis, promote survival of nerve cells and inhibit formation of glial scar; BBB grade of treated animals is increased remarkably; and the western medicine has remarkable promotion effect on functional recovery of locomotion after fracture. Compared with methylprednisolone as a common drug for treating fracture, the western medicine compound is wider in administration window, is lasting in treatment effect and better in long-term effect.

The present invention falls within the field of medical technology, and in particular relates to the use of a compound as shown in formula (I). In particular, the present invention relates to the use of the compound as shown in formula (I) in the preparation of a pharmaceutical composition for preventing and/or treating a nerve injury, or relieving a nerve injury-associated symptom, and further relates to the use thereof in the preparation of a healthcare product for protecting an injured nerve and/or improving motor function. After a nerve injury has occurred, the compound can reduce the production of pro-inflammatory cytokine, decrease the level of apoptosis, promote the survival of neuron, inhibit the formation of glial scar, and has a significant effect in promoting the recovery of motor function.

The invention provides a preparation method of olfactory ensheathing cell photocuring nerve repair hydrogel. The preparation method specifically comprises the following steps: preparing a hydrogel composite scaffold; mixing the hydrogel composite scaffold with a DMEM/F-12 culture medium containing fetal calf serum to obtain a composite culture medium; and culturing the olfactory ensheathing cells by using the composite culture medium to obtain the olfactory ensheathing cell light-cured neural restoration hydrogel. Compared with traditional olfactory ensheathing cells, the olfactory ensheathing cell photo-curing nerve repair hydrogel provided by the invention can effectively improve the survival rate of the olfactory ensheathing cells, also can fill spinal cord tissue defects and integrate with peripheral tissues, inhibit inflammatory response and glial scar formation, induce nerve fiber regeneration, and improve the survival rate of the olfactory ensheathing cells. The recovery of the motion function after spinal cord injury can be promoted to a certain extent.

The present invention is based on the capacity of the Olfactory Ensheathing Glia (OEG) to foster axonal regeneration in the adult mammalian central nervous system (CNS). This specific capacity is probably due to a combination of several factors, such as the molecular composition of cellular membrane and/or the capacity to secrete some molecules; combined with the capacity to reduce glial scar and accompany new growing axon in the damaged CNS. We have developed immortalised cell lines from primary human OEGs. The cells were cultured from post-mortem human tissue from donors and immortalised using a reversible system. Some of these OEG human clonal cell lines were selected by their ability to promote axonal regeneration from adult rat retinal ganglion neurons in a similar fashion to primary OEGs. These cell lines, alone or in pharmaceutical compositions comprising these cells, may be used to repair neuronal damage in the CNS.