Digestive Disease Model Construction Service for Exosome Functional Research

The huge changes in diet structure and the accelerated pace of life caused by the rapid development of the current social economy have become an important reason for the high incidence of digestive system diseases (DSDs). DSDs involve a wide range of organic and functional diseases of organs, including the stomach, intestine, liver, pancreas, etc. Common DSDs include non-alcoholic steatohepatitis (NASH), gastric ulcer (GU), colitis, pancreatitis, etc. In recent years, with the continuous updating of exosome research technology and the deepening of exosome research, a large number of scientists have shown that exosomes have great application prospects in the diagnosis or treatment of DSDs. To speed up the translation of these research results to the clinic, it is very important to choose what kind of animal model. Creative Biolabs has been paying attention to the research progress of exosomes in the treatment or diagnosis of DSDs. We can provide various DSD animal models and follow-up curative drug efficacy research and evaluation services for global customers.

Fig.1 A schematic diagram of the experimental design was followed to investigate the immunomodulatory effects of MSC-Exos in DSS-induced colitis. (Heidari, 2022)

Creative Biolabs Digestive System Disease Model Library for Exosome Functional Research

We can provide including but not limited to the following DSD animal models for exosome functional research.

DSD Animal Models	Method	Modeling Mechanism	Applicable Animals	Model Features
NASH animal models	Diet deficient in methionine and choline	Deficiency of methionine and choline can lead to abnormal mitochondrial oxidation function and decreased synthesis of very low-density lipoprotein, which aggravates inflammation and promotes the early development of liver fibrosis	Mouse, rat	The method is simple to operate and has good repeatability, and can induce macrovesicular steatosis, inflammation, and fibrosis in mice in a short period, all of which are similar to human NASH.
	Carbon tetrachloride induction	Carbon tetrachloride induces the occurrence of oxidative stress in the liver and the continuous production and accumulation of harmful lipid and protein peroxidation products, destroying liver cell structure and function.	Mouse	The modeling time is short and the modeling success rate is high. This model is suitable for the study of liver fibrosis.
	Leptin or leptin receptor gene-deficient mice fed a diet deficient in methionine and choline	Defects in leptin or leptin receptors lead to increased food intake, decreased energy expenditure, and increased fat synthesis. A diet deficient in methionine and choline could induce a transition from hepatic steatosis to steatohepatitis in these mice.	Mouse	Compared with simple diet induction, the modeling time is shorter. The model can replicate almost all graded phenotypes of NASH.
GU animal models	Absolute ethanol induction	Absolute ethanol is very corrosive and can directly damage the gastric mucosal barrier, causing obvious damage to the gastric mucosa.	Rat	The ulcer appearance, histological characteristics, healing, and recurrence process of this model are similar to those of human gastric mucosal injury.
GU animal models	Indomethacin or aspirin induction	Indomethacin or aspirin can weaken the function of the gastric mucosal barrier by inhibiting gastric mucosal cyclooxygenase, and eventually induce excessive gastric acid concentration and induce ulcers.	Rat	The model has good repeatability and is suitable for exploratory research on drugs for GU treatment.
Colitis animal models	Dextran Sodium Sulfate (DSS) induction	DSS destroys epithelial cells, causing nonspecific immune cells to release inflammatory factors.	Mouse, rat	The method has good repeatability and high modeling success rate and can replicate changes in the acute and remission phases of human colitis.
Colitis animal models	Trinitro benzenesulfonic acid (TNBS) induction	The absolute ethanol used to dilute TNBS effectively broke the intestinal barrier, allowing TNBS to interact with colonic tissue proteins, resulting in the release of inflammatory factors by non-specific immune cells.	Mouse, rat	Modeling costs are lower. The course of colitis in this model is rapid and can cause persistent damage to the distal colon.
Pancreatitis animal models	Sodium taurocholate induction	Sodium taurocholate is readily perfused retrogradely into the pancreas (similar to bile reflux), injuring the pancreas and inducing acute pancreatitis.	Mouse, rat	This model is a mature model of acute necrotizing pancreatitis.
Pancreatitis animal models	Combined induction of caerulein and lipopolysaccharide (LPS)	Caerulein can promote the secretion of a large amount of trypsin and cause autolysis of pancreatic acini. LPS can continuously activate inflammatory cells to release inflammatory factors and aggravate pancreatitis.	Mouse, rat	This method can adjust the severity of acute pancreatitis by adjusting the dosage of caerulein.

Creative Biolabs is a world-leading exosome technology service provider. In terms of in vivo research on exosomes, we can provide a wide variety of DSD animal models to accelerate your project progress. Please do not hesitate to contact us with your needs. Our professional team will provide you with one-stop services including exosome extraction, exosome identification, exosome engineering, exosome labeling, and in vivo and in vitro verification of exosomes with first-class services.

Reference

Heidari, N.; Abbasi-Kenarsari, H.; et al. Regulation of the Th17/Treg balance by human umbilical cord mesenchymal stem cell-derived exosomes protects against acute experimental colitis. Experimental Cell Research. 2022. 419(1):113296.

Plant Exosome Isolation