CN105497901A - Application of calcium-activated chloride channel antagonist - Google Patents
Application of calcium-activated chloride channel antagonist Download PDFInfo
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- CN105497901A CN105497901A CN201510928370.6A CN201510928370A CN105497901A CN 105497901 A CN105497901 A CN 105497901A CN 201510928370 A CN201510928370 A CN 201510928370A CN 105497901 A CN105497901 A CN 105497901A
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Abstract
The invention belongs to the field of medicine and particularly relates to application of a calcium-activated chloride channel antagonist, in particular to application of the calcium-activated chloride channel antagonist in preparing medicine for treating nerve demyelination diseases. According to the application, it is proposed for the first time that the calcium-activated chloride channel antagonist is used for preparing the medicine for treating nerve demyelination diseases, and the diseases such as multiple sclerosis, acute infectious polyradiculoneuritis, multifocal leukoencephalitis, sub-acute sclerosing panencephalitis, pons central type myelin disintegrative disorder, progressive subcortical ischemic encephalopathy, senile dementia and schizophrenia can be safely, efficiently and stably treated.
Description
Technical field
The invention belongs to field of medicaments, specifically the purposes of calcium-activated potassium current antagonist.
Background technology
Nerve fiber is divided into amyelinated nerve fiber and Medullated nerve fibre.Medullated nerve fibre is as vegetative nerve preganglionic fibre and larger somatic nerve fiber, and its axon has an epitheca, is called myelin.Myelin is made up of the cell membrane of myelin cell.The myelin cell of nervus centralis is few dendron glial cell, the myelin of peripheral nerve fiber is that the cell membrane executing ten thousand Schwann Cells is formed.Myelin is made up of lipid and protein.Axon can be protected to have again insulating effect to neural impulse, can the conduction of accelerator nerve impulsion.The fiber conduction of impulse that myelin is thick is also fast.When myelin is destroyed, conduct velocity.Nerve conduction is also by the impact of temperature, and when myelinoclasis, the rising of body temperature can cause conduction block.
The effect of myelin is neuroprotective unit and makes neural impulse on neuron, obtain very fast transmission, so the depigmentation of myelin can make the transmission of neural impulse be affected.The neural myelin of acute demyelinating disease can regenerate, and speed is comparatively rapid, and degree is comparatively complete, although the myelin of regeneration is thinner, general little on the impact of functional rehabilitation.Chronic demyelinating neuropathy, due to the regeneration Schwann cell had significant proliferation of demyelination and myelin repeatedly, nerve can be thicker, and have Quantifying axonal loss, and therefore functional rehabilitation is incomplete.The neural myelin of acute demyelinating disease can regenerate, and speed is comparatively rapid, and degree is comparatively complete, although the myelin of regeneration is thinner, general little on the impact of functional rehabilitation.Chronic demyelinating neuropathy, due to the regeneration Schwann cell had significant proliferation of demyelination and myelin repeatedly, nerve can be thicker, and have Quantifying axonal loss, and therefore functional rehabilitation is incomplete.Demyelination is that a class cause of disease is not identical, clinical manifestation is different but has the acquired illness of roughly the same feature, and the pathological change of its feature is the myelinoclasis of nerve fiber and neurocyte keeps complete relatively.I.e. dysmyelination type and myelinoclasis type.Dysmyelination type demyelination is the dysmyelination that heredity metabolize defect causes, mainly comprise the abnormal leukodystrophy caused of myelin phospholipid metabolism, as metachromasy leukoencephalopathy, alba cavernous transformation, addison-Schilder disease etc.Myelinoclasis type demyelination is acquired demyelination.
Its common disease comprises: 1. immune-mediated, as multiple sclerosis, samples polyradiculoneuritis; 2. viral infection, leukoencephalitis as multifocal in Progressive symmetric erythrokeratodermia, subacute sclerosing panencephalitis; 3. malnutrition, as Central pontine type myelin disintegrate disease; 4. anoxia, as ischemic encephalopathy under demyelination disease, Progressive symmetric erythrokeratodermia cortex after Delayed onset anoxia.The demyelination that during the general demyelination of diagnosis clinically, many fingers are immune-mediated, comprises multiple sclerosis, samples polyradiculoneuritis etc.The Therapeutic Method that there is no at present, main employing hormone therapy and neurotrophy, unsatisfactory curative effect.
Summary of the invention
The present invention finds the novelty teabag of calcium-activated potassium current antagonist by research, can be used for treatment nerve demyelination disease.
Niflumic acid, be the putative calcium-activated potassium current antagonist of one, be applied to clinical at present mainly as non_steroidal anti_inflammatory drug, curative effect is better than other anti-inflammation analgesia medicines, can be used for gerontal patient.For acute and chronic arthritis and non-arthritis, wound and post-surgical inflammation, also can be used for bronchitis, pneumonia, acute shallow table thrombophlebitis etc.
The invention provides the purposes of calcium-activated potassium current antagonist in preparation treatment nerve demyelination disease medicament.
Described nerve demyelination disease comprises ischemic encephalopathy, senile dementia, schizophrenia under multiple sclerosis, samples polyradiculoneuritis, multifocal leukoencephalitis, subacute sclerosing panencephalitis, Central pontine type myelin disintegrate disease, Progressive symmetric erythrokeratodermia cortex.
Described calcium-activated potassium current antagonist comprises, niflumic acid or T16Ainh-A01 type selective depressant.
Beneficial effect of the present invention is: calcium-activated potassium current antagonist has well anti-de-nerve demyelination symptom, is a kind of safe, efficient, stable medicine.
Detailed description of the invention
Below in conjunction with embodiment, the invention will be further described.
Niflumic acid, be the putative calcium-activated potassium current antagonist of one, be applied to clinical at present mainly as non_steroidal anti_inflammatory drug, curative effect is better than other anti-inflammation analgesia medicines, can be used for gerontal patient.For acute and chronic arthritis and non-arthritis, wound and post-surgical inflammation, also can be used for bronchitis, pneumonia, acute shallow table thrombophlebitis etc.
The present embodiment provides the purposes of calcium-activated potassium current antagonist in preparation treatment nerve demyelination disease medicament.
Described nerve demyelination disease comprises ischemic encephalopathy, senile dementia, schizophrenia under multiple sclerosis, samples polyradiculoneuritis, multifocal leukoencephalitis, subacute sclerosing panencephalitis, Central pontine type myelin disintegrate disease, Progressive symmetric erythrokeratodermia cortex.
Described calcium-activated potassium current antagonist is for niflumic acid or T16Ainh-A01 type selective depressant.
(1) experimental animal: HM mice, is provided by Wuhan University's animal experimental center.
(2) test material: niflumic acid, traditional Chinese medicines group provides, lot number: 20150507; T16Ainh-A01 is provided by ocean Science and Technology Ltd. of Beijing China, lot number: 20141209.
(3) test method: adopt bisoxalydihydrazone (CPZ, cuprizone) to prepare mice demyelination schizophrenia model, Kunming male mice 40, is divided into 4 groups at random, often organizes 10.Normal group, feeds chow diet; Model group, is fed with the feedstuff of the bisoxalydihydrazone (CPZ) of 0.2%, continuous 3 weeks; Model+niflumic acid group, ig, 20mg/kg, once a day; Model+T16Ainh-A01 group, ig, 2mg/kg, once a day.After testing 3 weeks, carry out open field test, forced swim test, water maze laboratory.
(4) statistical procedures: adopt SPSS10.0 to carry out statistical analysis as seen.Measurement data represents with (χ ± S), and result carries out t inspection; Enumeration data adopts X 2 test.P<0.05 is significant difference.
(5) result of the test: open field test result visible normal group center lattice percentage rate is 25.3%, model group center lattice percentage rate is 10.9%, the center lattice percentage rate of niflumic acid is 17.3%, the center lattice percentage rate of T16Ainh-A01 is 22.6%, hints model group mice is sought ability to study and declines, and niflumic acid can significantly improve such symptom; Forced swimming result is visible, and normal group non-swimming time is 192s, and model group non-swimming time is 286s, shows that demyelination mice feeling of despair strengthens.Niflumic acid group non-swimming time is 176.9s, T16Ainh-A01 non-swimming time is 126.9s, shows that calcium-activated potassium current blocker significantly can improve the mental status of mice.Water maze laboratory result is visible, in normal group 120s, cross-platform number of times is 3.06 times, and model group is 1.54 times, and niflumic acid group is 2.66 times, T16Ainh-A01 group is 2.43 times, shows that calcium-activated potassium current tool is significantly improved the memory ability of nerve injury mice.The results are shown in 1.
Table 1 is on the impact of Mental Subnormality mice study desire, desire of seeking survival and memory
* * p<0.01 compared with normal group; ##p<0.01 compared with model group.
The above is only the preferred embodiment of the present invention; it should be pointed out that for those skilled in the art, under the premise without departing from the principles of the invention; can also make some improvement or distortion, these improve or distortion also should be considered as protection scope of the present invention.
Claims (3)
1. the purposes of calcium-activated potassium current antagonist in preparation treatment nerve demyelination disease medicament.
2. purposes according to claim 1, is characterized in that: described nerve demyelination disease comprises ischemic encephalopathy, senile dementia, schizophrenia under multiple sclerosis, samples polyradiculoneuritis, multifocal leukoencephalitis, subacute sclerosing panencephalitis, Central pontine type myelin disintegrate disease, Progressive symmetric erythrokeratodermia cortex.
3. purposes according to claim 1, is characterized in that: described calcium-activated potassium current antagonist comprises, niflumic acid or T16Ainh-A01 type selective depressant.
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| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN201510928370.6A CN105497901A (en) | 2015-12-15 | 2015-12-15 | Application of calcium-activated chloride channel antagonist |
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| CN201510928370.6A CN105497901A (en) | 2015-12-15 | 2015-12-15 | Application of calcium-activated chloride channel antagonist |
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Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| JP2002003402A (en) * | 2000-06-27 | 2002-01-09 | Japan Science & Technology Corp | Agent for controlling death of cell |
| WO2008046014A1 (en) * | 2006-10-12 | 2008-04-17 | Remedy Pharmaceuticals, Inc. | Treatment of alzheimer's disease using compounds that reduce the activity of non-selective ca++- activated atp-sensitive cation channels regulated by sur1 receptors |
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- 2015-12-15 CN CN201510928370.6A patent/CN105497901A/en active Pending
Patent Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| JP2002003402A (en) * | 2000-06-27 | 2002-01-09 | Japan Science & Technology Corp | Agent for controlling death of cell |
| WO2008046014A1 (en) * | 2006-10-12 | 2008-04-17 | Remedy Pharmaceuticals, Inc. | Treatment of alzheimer's disease using compounds that reduce the activity of non-selective ca++- activated atp-sensitive cation channels regulated by sur1 receptors |
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Application publication date: 20160420 |
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