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Method for improving protective effect of creatine on excitatory neurotoxicity

A neurotoxic and excitatory technology, applied in the field of biomedicine, can solve the problems of not mentioning Cr, ignoring the catalytic function of CK, limited therapeutic effect, etc., to achieve the effect of improving the protective effect

Active Publication Date: 2019-05-17
王铁鹏
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

What is the reason for the limited therapeutic effect of Cr? There is no targeted research report
Literature survey found that in many researches trying to improve neurodegeneration through Cr, the researchers mainly focused on factors such as dose, time, and administration method of Cr, but did not mention whether the addition of Cr can really be catalyzed to form PCr, ignoring whether the catalytic function of CK is normal

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  • Method for improving protective effect of creatine on excitatory neurotoxicity
  • Method for improving protective effect of creatine on excitatory neurotoxicity
  • Method for improving protective effect of creatine on excitatory neurotoxicity

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Embodiment Construction

[0023] The technical solution of the present invention will be described in further detail below in conjunction with the accompanying drawings and specific embodiments.

[0024] The technical terms used in the present invention are put into Chinese and English contrast: creatine (Creatine, Cr), creatine kinase (Creatine kinase, CK), nitrosoglutathione (S-Nitrosoglutathione, GSNO), GSNO reductase ( S-nitrosoglutathione reductase, GSNOR), nerve cell cytoplasmic creatine kinase (Creatine kinasebrain type, CKBB), nerve cell mitochondrial creatine kinase (Mitochondrial creatine kinase, CKMT), phosphocreatine (phosphocreatine, PCr), 2, 4-Dinitrofluorobenzene (2,4-Dinitrofluorobenzene, DNFB), Cerebellar granule neuron (CGN), Alzheimer's disease (Alzheimer's disease, AD), Parkinson's disease (Parkinson's disease , PD), Huntington's disease (Huntington's disease, HD), amyotrophic lateral sclerosis (Amyotrophic lateral sclerosis, ALS).

[0025] 1. Experimental method

[0026] 1.1 Exog...

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Abstract

The invention discloses a method for improving the protective effect of creatine on excitatory neurotoxicity, and establishes an exogenous nitric oxide donor GSNO to treat an excitatory neurotoxicitymodel of SH-SY5Y cells. It is proved that a simple creatine factor has the protective effect on the excitatory neurotoxicity by utilizing the model, but the effect is limited. In the SH-SY5Y model treated by the GSNO, both nerve type creatine kinases CKBB and CKMT are modified by nitrosation, and the protein content and enzyme activity are significantly decreased after modification; the nitrosylated modification enzyme GSNOR is removed through overexpression, the nitrosylated modification of the CKBB and CKMT can be significantly reduced, and the content and activity of CKBB and CKMT can be removably restored. By combining the method with the nitrosylated modification removing scheme of the nerve type creatine kinases, the protective effect of creatine on excitatory neurotoxicity can be removably improved.

Description

technical field [0001] The invention belongs to the technical field of biomedicine, and relates to a method for improving the protective effect of creatine on excitatory neurotoxicity, in particular to a denitrosylation modification method of neural creatine kinase (CKBB and CKMT) in enhancing creatine Drug application in neuroprotective effect. Background technique [0002] Neurodegenerative diseases are a group of neurological diseases that result in progressive functional variation and death of nerve cells, leading to abnormal behavior and dysfunction of patients, and premature death, including Alzheimer's disease (AD), Parkinson's disease disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), etc. Excitotoxicity is a common pathway leading to late neuronal death in the pathogenesis of neurodegenerative diseases. Among them, energy depletion caused by processes such as mitochondrial respiratory chain inhibition, glycolysis inhibition, and energy c...

Claims

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Application Information

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IPC IPC(8): A61K31/198A61P25/28
Inventor 王铁鹏陈畅张婷赵博田云云李巧彦张倩孙悦
Owner 王铁鹏
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