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Application of KCa3.1 channel specific inhibitor in preparation of drug for treating AD (Alzheimer's disease)

An inhibitor and specific technology, applied in the direction of drug combination, neurological diseases, active ingredients of amides, etc., can solve problems such as inability to delay the disease process

Inactive Publication Date: 2018-08-21
SHANGHAI JIAOTONG UNIV SCHOOL OF MEDICINE
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0003] The existing FDA-approved AD treatment drugs mainly target acetylcholinesterase and N-methyl-D-aspartate receptors, which can only relieve symptoms, but cannot delay the progress of the disease

Method used

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  • Application of KCa3.1 channel specific inhibitor in preparation of drug for treating AD (Alzheimer's disease)
  • Application of KCa3.1 channel specific inhibitor in preparation of drug for treating AD (Alzheimer's disease)
  • Application of KCa3.1 channel specific inhibitor in preparation of drug for treating AD (Alzheimer's disease)

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0026] Example 1. Detection of Cognitive Function Behavior

[0027] In the present embodiment, using the Morris water maze behavioral experiment, the control group (WT), the control group (WT+Senicapoc) using the inhibitor Senicapoc, the AD animal model (APP / PS1), and the control group (WT+Senicapoc) using the inhibitor Senicapoc Four groups of mice in the AD animal model (APP / PS1+Senicapoc) were tested for cognitive function behavior. The AD animal model used 15-month-old APP / PS1 mice, and the control group used 15-month-old C57BL / 6 mice. The dose of the inhibitor Senicapoc was 120 mg / kg / day, once a day, and treated by intragastric administration for 4 weeks, and obtained Such as figure 1 The plateau latency shown in A, figure 1 Percentage of swimming distance in the target quadrant for each group of mice shown in B, and, figure 1 The experimental data of the percentage of swimming time in the target quadrant of each group of mice shown in C (Data represent means ± SEM (n ...

Embodiment 2

[0029] Example 2. Detection of neuron survival in the brain

[0030] In this example, immunofluorescent staining was used to compare the control group (WT), the control group (W+Senicapoc) with the inhibitor Senicapoc, the AD animal model (APP / PS1), and the AD animal model with the inhibitor Senicapoc Four groups of mice (APP / PS1+Senicapoc) underwent NeuN in the CA1 region + neuronal expression. The AD animal model used 15-month-old APP / PS1 mice, and the control group used 15-month-old C57BL / 6 mice. The dose of the inhibitor Senicapoc was 120 mg / kg / day, once a day, and treated by intragastric administration for 4 weeks. figure 2 NeuN in the CA1 region shown in A + neuron expression maps, and figure 2 The experimental data of the number of neurons shown in B (Quantification of neuron number / 0.01mm 2 in hippocampus (n=6-8). Data represent mean±SEM. *p<0.05, **p<0.01 (one-way ANOVA followed by Dunnett’s post hoc test). Scale bars: 25 μm.).

[0031] figure 2 A and figur...

Embodiment 3

[0032] Example 3. Detection of Microglia Activation in the Brain

[0033] In this example, using immunofluorescent staining, the control group (WT), the control group (WT+Senicapoc) using the inhibitor Senicapoc, the AD animal model (APP / PS1), and the AD animal model using the inhibitor Senicapoc Four groups of mice (APP / PS1+Senicapoc) performed IBA-1 in the hippocampal region of the brain +Activated microglial expression. The AD animal model used 15-month-old APP / PS1 mice, and the control group used 15-month-old C57BL / 6 mice. The dose of the inhibitor Senicapoc was 120 mg / kg / day, once a day, and treated by intragastric administration for 4 weeks. image 3 A shows the hippocampal region of the brain IBA-1 + activated microglia expression map, and image 3 The experimental data of the number of activated microglial cells shown in B (Quantification ofactivated microglial number / 0.01mm 2 in hippocampus (n=6-8). Data represent mean±SEM. ** p<0.01 (one-way ANOVA followed by Du...

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Abstract

The invention provides an application of a KCa3.1 channel specific inhibitor, particularly an inhibitor Senicapoc, in preparation of a drug for treating the AD (Alzheimer's disease).

Description

technical field [0001] The invention relates to a KCa3.1 channel-specific inhibitor, especially the application of the inhibitor Senicapoc in the preparation of drugs for treating Alzheimer's disease. Background technique [0002] Alzheimer's disease (AD) is the most common neurodegenerative disease in the elderly characterized by progressive cognitive dysfunction. It is a complex heterogeneous disease involving multiple factors. Its genetic and environmental interaction mechanisms and drug targets Research has always been an important area of ​​life medical research today. [0003] The existing FDA-approved AD treatment drugs mainly target acetylcholinesterase and N-methyl-D-aspartate receptors, which can only alleviate symptoms, but cannot delay the progress of the disease. [0004] Therefore, in-depth study of the pathophysiological mechanism of AD and the search for new drug targets have important theoretical significance and practical value. Contents of the invention...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K31/16A61P25/28
CPCA61K31/16
Inventor 虞志华陈红专韦天娇
Owner SHANGHAI JIAOTONG UNIV SCHOOL OF MEDICINE
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