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Application of FUNDC1 in treating acute respiratory distress syndrome and belongs to technical field of biology

A technology of FUNDC1, 1.FUNDC1, applied in the field of application in the treatment of acute respiratory distress syndrome, capable of solving damage, sepsis organs and other problems

Pending Publication Date: 2020-05-12
PEKING UNION MEDICAL COLLEGE HOSPITAL CHINESE ACAD OF MEDICAL SCI
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0004] Under normal circumstances, the heightened inflammatory response can be eliminated at the right time to avoid harm to the body; however, once the situation gets out of hand, the overactivated inflammasome will produce a large amount of pro-inflammatory cytokines, eventually leading to sepsis and organ damage

Method used

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  • Application of FUNDC1 in treating acute respiratory distress syndrome and belongs to technical field of biology
  • Application of FUNDC1 in treating acute respiratory distress syndrome and belongs to technical field of biology
  • Application of FUNDC1 in treating acute respiratory distress syndrome and belongs to technical field of biology

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0038] Embodiment 1 establishes animal model

[0039] Wild-type 6-week-old adult male C57BL / 6J mice and FUNDC1 knockout (FUNDC1-KO) mice were provided by the Department of Biochemistry and Molecular Biology, Institute of Zoology, Chinese Academy of Sciences. Genomic DNA was detected from the tail by PCR amplification to detect the genotype of the knockout mice. Compared with littermates, FUNDC1-KO were not statistically different in sex, age of week and body weight. All experimental animals have health certificates. All FUNDC1-KO and their littermates were kept in a constant temperature (20–24°C) and specific pathogen-free facility. According to the "Guide for the Care and Use of Laboratory Animals" issued by the National Institutes of Health, the mice were allowed free access to food and water, and were kept in a normal state on a 12-h light-dark cycle. All procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Peking Union Medical College Hos...

Embodiment 2

[0041] Embodiment 2 lung histopathology

[0042] Immediately after the mice were sacrificed, right lower lung tissues were collected and fixed in 10% formalin solution. Tissue samples were dehydrated and embedded in paraffin. Serial paraffin sections (4um) were obtained and kept at 37°C for more than 12h. Sections were immersed in three consecutive washes of xylenol for 5 min to remove paraffin, then hydrated with five consecutive washes of decreasing alcohol content: 100%, 95%, 80%, 70%, 50%, and finally with deionized Wash with water. Then the tissue paraffin sections were stained with HE. Changes in tissue structure were observed using a light microscope. Two professional pathologists were invited to score lung lesions according to a blinded method. The scoring criteria are based on six pathological features: (1) alveolar edema; (2) interstitial edema; (3) inflammatory cell infiltration; (4) lung wall thickening; (5) atelectasis; (6) Transparent film. Each of the pat...

Embodiment 3

[0044] Example 3 Pulmonary tissue inflammatory infiltration and lung injury

[0045] Neutrophils are an important marker of leukocyte inflammatory response in acute lung injury. The inventors also performed neutrophil counts in alveolar lavage fluid using HE stain. The result is as figure 2 As shown in A, compared with the WT+LPS group and the FUNDC-1 KO or normal control group, the FUNDC-1 KO+LPS group had more neutrophil infiltration (1.08±0.08×10 3 / ml vs. 0.75±0.07×10 3 / ml vs. 0.20±0.04×10 3 / ml vs. 0.19±0.03×10 3 / ml, P<0.05).

[0046] In addition, the inventor detects the myeloperoxidase (MPO) activity (Catalog# A044-1-1 , Jiancheng Biological Engineering Company, Nanjing). MPO is a marker enzyme of neutrophil activation, and the change of its content reflects the infiltration of neutrophils. The result is as figure 2 As shown in B, MPO concentration presents the same expression trend. Compared with WT+LPS group, FUNDC1 KO group or normal control group, FUND...

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Abstract

The invention discloses an application of FUNDC1 in treating acute respiratory distress syndrome and belongs to the technical field of biology. The present invention provides the application of the FUNDC1 in preparing products for preventing and / or treating inflammatory diseases. The mechanism of the FUNDC1 in preventing and / or treating inflammatory diseases is mainly to reduce lung injury by mediating mitochondrial autophagy to inhibit activation and expansion of inflammatory reactions induced by an ROS-NLRP3 signaling pathway. The invention provides the application of the FUNDC1 in preparingproduct for preventing and / or treating acute respiratory distress syndrome. The product provided by the invention can reduce lung injury by inhibiting inflammatory reactions by promoting autophagy during ARDS period. The FUNDC1 is expected to become a new target for ARDS treatment and has a wide application prospect.

Description

technical field [0001] The invention relates to the field of biotechnology, in particular to the application of FUNDC1 in the treatment of acute respiratory distress syndrome. Background technique [0002] The etiology of acute respiratory distress syndrome (ARDS) is complex, and its pathogenesis has not been fully elucidated. Numerous studies have shown that the inflammatory response in the lung is the most important cause of ALI / ARDS. The activation of innate and adaptive immunity leads to a series of inflammatory responses, and the release of a large number of cytokines and inflammatory mediators leads to the aggravation of lung injury. The end result of this uncontrolled inflammatory response in the lung is damage to alveolar epithelial cells (AEC) and capillary endothelial cells, which in turn leads to alveolar hemorrhage, pulmonary edema formation, and hyaline membrane production. [0003] Autophagy is a lysosome-dependent biological process for degrading intracellul...

Claims

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Application Information

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IPC IPC(8): A61K38/17A61P11/00A61P31/00A61P29/00
CPCA61K38/177A61P11/00A61P31/00A61P29/00
Inventor 苏龙翔潘盼隆云刘大为周翔王小亭何怀武
Owner PEKING UNION MEDICAL COLLEGE HOSPITAL CHINESE ACAD OF MEDICAL SCI
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