Fibrosis Disease Model Construction Service

Fibrosis Disease Model Construction Service

Construct Stable Models for Studying Glycobiology-related Fibrotic Diseases

CD BioGlyco is an unparalleled carbohydrate research company that helps clients solve various difficulties and problems encountered in carbohydrate development and research. With the development of Glycomics and Glycoproteomics, diseases related to abnormal protein glycosylation have attracted great attention from researchers. CD BioGlyco has a professional team dedicated to the study of Glycobiology Disease Model, providing first-class Glycobiology Disease Model Construction Service, Custom In Vivo Glycobiology Disease Model Service, In Vivo Glycobiology Disease Model Screening Service, and In Vitro Glycobiology Disease Model Screening Service. Our Techniques for In Vivo Glycobiology Disease Model Development include:

Fibrosis is characterized by tissue scarring and is the root cause of various organ diseases, but effective treatments are often lacking. The construction of animal models related to human diseases has attracted increasing attention in the industry to optimize the study of the causes of fibrosis. At CD BioGlyco, we help clients construct the following models to study the molecular mechanisms of changes in protein glycosylation during the formation of pulmonary fibrosis, liver fibrosis, etc.

Construct a variety of fibrosis disease models for clients. (CD BioGlyco)

  • Carbon tetrachloride (CCL4)-induced fibrosis model

With the occurrence of liver fibrosis, the transcription level of sugar-related genes involved in protein glycosylation modification and the expression level of glycosyltransferase and glycosidase in liver cells have changed to varying degrees, which directly affects the glycosylation modification of glycoproteins in liver cells. We construct a CCl4-induced fibrosis model to assist clients in studying the molecular mechanism of protein glycosylation changes during the formation of liver fibrosis from the perspective of glycomics, providing a theoretical basis for the treatment of liver fibrosis.

  • Thioacetamide (TAA)-induced fibrosis model

TAA is a compound widely used to simulate the damage caused by the pathogenesis of liver fibrosis. The mechanism of TAA-induced chronic liver damage is to affect protein synthesis and enzyme metabolism in hepatocytes. The changes in histology and biochemical metabolism are very similar to those of human cirrhosis caused by various causes. The induced liver fibrosis is more stable and persistent.

  • High-fat & cholesterol diet (HFCD)-induced fibrosis model

HFCD shows increased intrahepatic lipid deposition, liver index, and liver enzyme levels, accompanied by macrovesicular steatosis, severe hepatocyte ballooning, and diffuse inflammatory infiltration. We help clients build HFCD models for the study of hepatocyte ballooning, inflammation, and fibrosis.

  • Streptozotocin (STZ) -induced pulmonary fibrosis

Diabetes induces the accumulation of advanced glycation end products in the lungs. We help clients construct STZ-induced diabetic mice to study the expression of advanced glycation end products.

  • N-nitrosodiethylamine (DEN)-induced liver fibrosis model

DEA binds to DNA, RNA, and many proteins, causing DNA damage and affecting RNA transcription. We provide a DEN-mediated liver cancer model to simulate the tumorigenesis process.

Publication

Technology: CCl4-induced liver fibrosis mouse model

Journal: Saudi Journal of Biological Sciences

IF: 4.4

Published: 2021

Results: In order to study the defensive effect of propolis on CCl4-mediated inflammatory and fibrotic signals, the authors constructed a CCl4-induced liver fibrosis mouse model. After oral administration of propolis supplements to mice in the experimental group for 4 weeks, histological and immunohistochemical evaluations were performed. The results showed that propolis significantly reduced free radical levels and pro-inflammatory cytokines in mice with liver fibrosis, eliminated CCl4-mediated pro-fibrotic signals, and inhibited the development of liver fibrosis.

Fig.1 Histological evaluation of propolis on CCl4-induced liver fibrosis in mice.Fig.1 Propolis treatment mitigated hepatic fibrosis induced by CCl4 in our mouse model. (Sayed, et al., 2021)

Applications

  • Use to develop diagnostic and monitoring tools for fibrotic diseases.
  • Construct model animals to test anti-fibrotic drugs related to glycobiological diseases.
  • Study the molecular and cellular mechanisms of abnormal glycosylation behind the progression of fibrotic diseases and identify potential therapeutic targets.
  • Prepare specific models based on specific diseases to analyze and develop personalized treatment strategies.

Advantages of Us

  • Our professional team of experts has rich expertise in disease models, bioengineering, and pharmacology, providing you with consultation, experimental design, and data analysis support for fibrosis disease models.
  • We provide CCL4, TAA, HFCD, STZ, and DEN-induced fibrosis model construction services to assist you in studying various fibrotic diseases related to abnormal glycosylation.
  • We use species that meet your needs (such as rats, and mice) to enhance the applicability of your research results.
  • The models we construct are rigorously validated to ensure the reliability of the results obtained.

Frequently Asked Questions

  • Why construct glycobiology disease models?

Glycans, like nucleic acids, are important bioinformatic molecules. Whether in basic life processes such as fertilization, development, growth, differentiation, or immunity or the occurrence and development of diseases, such as plant-pathogen interaction, pathogen infection, inflammation and autoimmune diseases, abnormal proliferation and metastasis of cancer cells, sugar chains play a specific recognition and mediation role. Models related to abnormal glycosylation are constructed to study the molecular mechanism of changes in protein glycosylation during disease occurrence.

  • What changes occur in protein glycosylation during liver fibrosis?

In liver fibrosis, the transcription levels of multiple glycosyltransferase genes are altered. The O-glycan synthesis pathway "Tn antigen→T antigen (core-1)→sialyl-T antigen" is activated during liver fibrosis. The expression of Fucα(1,6)GlcNAc, Fucα(1,3)LacNAc, bisecting GlcNAc, biantennary N-glycans, and Galβ(1,4)GlcNAc is upregulated on the membrane of activated hepatic stellate cells.

CD BioGlyco has developed a one-stop glycobiology disease model solution to assist you in studying the molecular mechanism of protein glycosylation changes in disease occurrence. If you are interested in constructing a glycobiology disease model, please feel free to contact us. Our professional team provides consulting and design services.

Reference

  1. Sayed, E.A.; et al. Induction of liver fibrosis by CCl4 mediates pathological alterations in the spleen and lymph nodes: The potential therapeutic role of propolis. Saudi Journal of Biological Sciences. 2021, 28(2): 1272-1282.
This service is for Research Use Only, not intended for any clinical use.

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