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Application of sodium valproate to preparation of medicine for restraining formation of glial scars and medical composition for restraining formation of glial scars

A technology of sodium valproate and glial scar, applied in the direction of drug combination, anhydride/acid/halide active ingredients, blood diseases, etc., to achieve the effect of inhibiting activation, inhibiting the formation of glial scar, and promoting recovery

Inactive Publication Date: 2019-08-06
SUZHOU UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0006] In the prior art, no studies have confirmed that sodium valproate

Method used

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  • Application of sodium valproate to preparation of medicine for restraining formation of glial scars and medical composition for restraining formation of glial scars
  • Application of sodium valproate to preparation of medicine for restraining formation of glial scars and medical composition for restraining formation of glial scars
  • Application of sodium valproate to preparation of medicine for restraining formation of glial scars and medical composition for restraining formation of glial scars

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0048] Protective effect of VPA on focal ischemic stroke in rats.

[0049] Male SD rats were randomly divided into a control group (sham operation group), a control administration group (VPA 250 mg / kg), a model group, and a model administration group (VPA 250 mg / kg), with 10 rats in each group. The rat model of transient middle cerebral artery occlusion (tMCAO) was established by suture method. After 90 minutes of MCAO, the rats in the control administration group and the model administration group were injected with VPA solution (250 mg / kg) intraperitoneally immediately, and the rats in the model group and the sham operation group were reperfused with a corresponding volume of normal saline immediately. After the first injection of VPA and normal saline, the second injection was completed at the same time the next day, and then once a day for a total of 28 days. The neurological symptoms of rats after reperfusion were scored by the Longa method once a week for four weeks. Th...

Embodiment 2

[0061] Inhibitory effect of VPA on the expression of glial scar-associated proteins GFAP, Neurocan and Phosphacan in ischemic rats.

[0062] Male SD rats were randomly divided into a control group (sham operation group), a control administration group (VPA 250mg / kg), a model group, and a model administration group (VPA 250mg / kg), with 3 rats in each group. The rat model of transient middle cerebral artery occlusion (tMCAO) was established by suture method. After 90 minutes of MCAO, the rats in the control administration group and the model administration group were injected with VPA solution (250 mg / kg) intraperitoneally immediately, and the rats in the model group and the sham operation group were reperfused with a corresponding volume of normal saline immediately. After the first injection of VPA and normal saline, the second injection was completed at the same time the next day, and then once a day for a total of 7 days. The brains were decapitated, and the expressions of ...

Embodiment 3

[0065] Inhibitory effect of VPA on the expression of related proteins GFAP, Neurocan and Phosphacan in an in vitro glial scar model.

[0066] When the primary astrocytes were cultured to a certain extent in a culture dish or a 24-well plate (accounting for about 80% of the holes in the culture dish or culture plate), they were divided into a control group (non-OGD) and a control administration group ( non-OGD+VPA), glial scar model group (OGD6h-Re24h) and model administration group (OGD6h-Re24h+VPA), the glial scar-associated proteins GFAP, Neurocan and Phosphacan were detected by western blot method or immunofluorescence method Express.

[0067] Figure 5 It is a schematic diagram of the effect of VPA on the expression of related proteins GFAP, Neurocan and Phosphacan in the in vitro glial scar model in Example 3, mean±SD, n=3, compared with the control group ##p<0.01; compared with the model group, * *p<0.01.

[0068] Figure 6 It is the immunofluorescence pattern of VPA...

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Abstract

The invention provides an application of sodium valproate to preparation of a medicine for restraining formation of glial scars. The structural formula of the sodium valproate is as shown in the description. Through experiment, the inventor finds that the sodium valproate has remarkable cranial nerve protecting effects, and can effectively restrain activation of primary astroglia cells and notablyrestrain the formation of the glial scars after the brain tissue of mice is damaged, so that the encephalatrophy volume of mice suffering from local cerebral ischemia can be obviously improved, the neurological symptoms of the mice can be notably improved, and restoration can be promoted; and the above situation indicates that the sodium valproate has important application value in preparation ofthe medicine for restraining the formation of the glial scars.

Description

technical field [0001] The invention relates to the application of sodium valproate in the preparation of medicines for inhibiting the formation of glial scars and its pharmaceutical composition. Background technique [0002] Stroke, also known as cerebrovascular accident, is a group of diseases whose main clinical manifestations are cerebral tissue ischemia and hemorrhagic injury symptoms. The disease has an acute onset, high disability rate and high mortality rate, and is one of the most important diseases that endanger human health in the world today. In recent years, the number of patients with cerebrovascular diseases in my country has increased year by year, and ischemic cerebrovascular diseases are the most common. At present, there are 1.2-1.5 million new cases of cerebral apoplexy each year in my country, 800-100 million deaths, about 75% of survivors become disabled, and the 5-year recurrence rate is as high as 41%. [0003] Stroke is a common central nervous sys...

Claims

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Application Information

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IPC IPC(8): A61K31/19A61P9/10A61P7/04A61P25/00A61P25/28
CPCA61K31/19A61P7/04A61P9/10A61P25/00A61P25/28
Inventor 张慧灵贺园园朱永铭周贤用
Owner SUZHOU UNIV
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