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Application of interleukin-37 to controlling fibrosis related diseases

A technology of interleukin and fibrosis, which can be used in metabolic diseases, sensory diseases, respiratory diseases, etc., can solve the problems that the regulation of fibrosis has not been involved in research, and achieve the effect of inhibiting fibrosis

Inactive Publication Date: 2018-09-18
TONGJI UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

However, the regulation of IL-37 on fibrosis has not been studied so far.

Method used

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  • Application of interleukin-37 to controlling fibrosis related diseases
  • Application of interleukin-37 to controlling fibrosis related diseases
  • Application of interleukin-37 to controlling fibrosis related diseases

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0030] The experimental steps include:

[0031] (1) Establish a mouse model of pulmonary fibrosis

[0032] Bleomycin-induced fibrosis in C57BL / 6 mice at a nasal inhalation dose of 15 mg / kg. The mice in the control group were injected with the same amount of normal saline, and the dose of IL-37 was 1.5 μg / kg by tracheal inhalation. In addition, in contrast, PBS buffer solution was added, and 1.5 μg / kg was also inhaled through the trachea. Dosing every other day from day 1 to day 21.

[0033] (2) After the four groups of mice were administered and cultured, the lungs were embedded in paraffin on the 21st day, and the paraffin sections were stained with Masson and HE, Western Blot, and qPCR to verify that IL-37 promotes pulmonary fibrosis through the TGF-β signaling pathway

[0034] Collection and preservation of bronchoalveolar lavage fluid: anesthetize the mice with 4% chloral hydrate 0.4 mg / kg, fix the limbs and head of the deeply anesthetized mice, and tilt the head and nec...

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Abstract

The invention experimentally proves that IL-37 can obviously enhance pulmonary fibrosis in vitro cell experiments and in vivo animal models. The invention further verifies experimentally that IL-37 promotes fibrosis through TGF-beta-ALK1 access. Therefore, through the discovery of the invention, the TGF-beta signal access can be inhibited by controlling the level of IL-37, and accordingly fibrosisof internal organs can be inhibited. In this way, IL-37 can serve as a treatment target site to treat fibrosis related diseases, such as idiopathic pulmonary fibrosis, ischemic heart diseases, viralliver cirrhosis and acute pancreatitis. According to the discovery of the invention, IL-37 has the obvious effect of worsening fibrosis in vitro fibrosis cell culture and in vivo animal models, meanwhile, IL-37 provides a direction for treatment of mice pulmonary fibrosis by serving as a new treatment target site for treating fibrosis related diseases. A more direct, effective and specific methodfor treating fibrosis is provided.

Description

technical field [0001] The invention belongs to the field of biotechnology, in particular to the application of an interleukin-37 (IL-37) in regulating fibrosis-related diseases. Background technique [0002] Fibrotic diseases include a wide variety of diseases, some with known etiologies and others with unknown etiologies. Affects multiple organ systems and causes severe morbidity and mortality. Myofibroblasts are the primary effector cells in fibrotic diseases characterized by persistent or progressive fibrosis. Myofibroblasts are also involved in normal wound healing by promoting wound closure and synthesis of extracellular matrix (ECM) proteins. The apparent disappearance of fibroblasts in granulation tissue heralds termination of the repair response of normal wound healing. This disappearance may involve the conversion of dedifferentiated myofibroblasts to a quiescent progenitor type or the clearance of apoptotic or dead myofibroblasts. In contrast, the persistence ...

Claims

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Application Information

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IPC IPC(8): A61K45/00A61P11/00A61P9/00A61P1/16A61P31/12A61P1/18A61P9/12A61P35/00A61P9/10A61P3/10A61P27/02G01N33/533
CPCA61K45/00A61P1/16A61P1/18A61P3/10A61P9/00A61P9/10A61P9/12A61P11/00A61P27/02A61P31/12A61P35/00G01N33/533
Inventor 寿娟娟杨天舒赵孟孟张姗姗曹晶晶
Owner TONGJI UNIV
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