Application of amlexanox in relieving experimental autoimmune encephalomyelitis (EAE), and experiment method

A technology of aminolexanol and aminolezanol, applied in the field of medicine, can solve problems such as unresearched

Inactive Publication Date: 2019-10-15
THE SECOND HOSPITAL OF HEBEI MEDICAL UNIV
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  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

However, the role of ALX in the immune regulation of central nervous system au...

Method used

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Embodiment Construction

[0038] The present invention will be described in further detail below.

[0039] The application of amlexanox in alleviating the onset of EAE, reducing the degree of spinal cord inflammatory cell infiltration and demyelination.

[0040] Amlesanox inhibits the phenotype and functional maturation of bone marrow-derived dendritic cells, and is associated with the TBK1 / Akt pathway.

[0041] When using experiments to verify that ammonia can inhibit the phenotype and functional maturation of dendritic cells derived from bone marrow, and that it is related to the TBK1 / Akt pathway, the experimental steps used are as follows:

[0042](1) The femur and tibia bone marrow of female C57BL / 6 mice was cultured under sterile conditions, induced to differentiate with GM-CSF, and immature BMDCs were cultured on the 8th day, and were randomly divided into three groups, among which LPS group was treated with LPS (1 μg / ml) to stimulate BMDC maturation, the ALX group was intervened with different...

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Abstract

The invention relates to an application of amlexanox in relieving experimental autoimmune encephalomyelitis (EAE) and relieving inflammatory cell infiltration and demyelination in a spinal cord. Whenthe result is specifically verified, a form of grouping experiments is adopted, and the verifying method specifically comprises the following three aspects: phenotype and functional maturation of bonemarrow-derived dendritic cells are inhibited by amlexanox, and the aspect is related to a TANK-binding kinase 1/Akt (TBK1/Akt) pathway; the condition of experimental autoimmune encephalomyelitis is modified by inhibiting the reaction of Th1/Th17 cells by amlexanox; and DC maturation in an experimental autoimmune encephalomyelitis spleen is inhibited by amlexanox through the TBK1/Akt pathway. According to the invention, the experiment result shows that the amlexanox (ALX) can inhibit DC maturation by inhibiting the TBK1/Akt conduction pathway and further inhibit differentiation of Th1 and Th17cells, so that a protective effect is achieved in EAE. The experiment provides an experimental basis for exploring pathogenesis of multiple sclerosis and searching for clinically safe and effective therapeutic drugs, and can be widely applied to the technical field of medicines.

Description

technical field [0001] The invention relates to the technical field of medicines, in particular to the application of amlexanox in alleviating the onset of EAE and its experimental method. Background technique [0002] Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease characterized by myelin-specific T cells infiltrating the central nervous system and triggering an inflammatory response cascade, leading to demyelination and neurological impairment. Previous studies have shown that Th1 and Th17 cells play an important role in the pathogenesis of MS and its animal model EAE. These antigen-specific Th1 and Th17 cells secrete inflammatory factors interferon-γ (interferon-γ, IFN-γ) and interleukin-17 (Interleukin-17, IL-17) in the pathological process of MS and EAE, respectively. IFN-γ has the function of activating DC, monocytes, macrophages and microglia. IL-17 can stimulate the production of chemokines and recruit neutrophils into the central nervous syste...

Claims

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Application Information

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IPC IPC(8): A61K31/436A61P25/00A61P29/00A61P37/00A61P9/10A61P37/02G01N15/14G01N23/02G01N23/2251G01N33/68
CPCA61K31/436A61P9/10A61P25/00A61P29/00A61P37/00A61P37/02G01N15/14G01N15/1434G01N23/02G01N23/2251G01N33/68
Inventor 全墨缘郭力侯慧清宋秀娟刘会佳邓晓红
Owner THE SECOND HOSPITAL OF HEBEI MEDICAL UNIV
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