Digestive System Disease Animal Model-Brain Case ()

Digestive system disease model

The characteristics of some animal diseases are very similar to those of human beings. In order to carry out better scientific research, more and more studies have been conducted using various animals as human disease models, especially animal models of digestive system disease model, such as viral hepatitis models. Immune hepatitis model; Gastric and intestinal ulcer models; Pancreatitis model; Diabetes model, etc.

Brain Case has established gastric acid secretion model, gastric ulcer disease, ulcerative colitis and gastrointestinal motivity disorder animal models, providing pharmacological efficacy evaluation services for digestive system disease, and facilitating drug research and development.

Digestive system disease model classification

• (1) Viral hepatitis model
  The common method is to replicate the hepatitis B model by injecting the serum of hepatitis B patients. However, most experimental animals are not sensitive to hepatitis A virus. Human hepatitis A has been reported in China after poisoning red-faced macaques, rhesus monkeys, humans and wild tree shrews. In recent years, it has been found that the characteristics of some duck hepatitis viruses are very similar to human hepatitis viruses, so the use of duck as a model of human hepatitis has also begun to increase.
• (2) Immune hepatitis model
  Antibodies against hepatocellular components are present in patients with chronic or prolonged hepatitis. In 1959, some people abroad immunized guinea pigs with Garver's adjuvant of liver tissue suspension and successfully induced hepatocyte degeneration and necrosis. It has also been reported that fractionated injection of liver membrane protein (LSP) with adjuvant produced an animal immune hepatitis model.
• (3) Gastric and intestinal ulcer models
  There are many ways to reproduce gastric and intestinal ulcers in animals, but the methods used are different, and the ulcer lesions caused by them are also different. Common methods are:

  a. Stress method causes stress ulcers in animals by various strong injurious stimuli (such as forced braking, hunger, cold, etc.). If the animal is immersed in cold water or placed in a stress box and constantly subjected to electrical stimulation, so that it is violently disturbed, the liquid can cause bleeding and ulcers of the gastric mucosa in a day. This method is simple and has a success rate of more than 99%.

  b. Taking or injecting a certain amount of histamine, gastrin, adrenal steroid, salicylate, serotonin, reserpine and butazone into animals by drug method can cause gastrointestinal ulcers in animals. If a small dose of histamine is given to guinea pigs for several days, it can cause ulcers in the stomach, duodenum and esophagus. For example, reserpine, serum tensin, aspirin can induce gastric ulcers in rats or mice.

  c.The cautery method uses electrodes to cauterize the stomach wall at the bottom of the stomach, which can cause gastric ulcer lesions like humans; Chronic ulcers can be caused by injecting concentrated acetic acid into the gastric wall of rats or applying it on the serous membrane of the gastric wall. The advantage of cautery method in replicating gastric and intestinal ulcer models is that it is simple and the site of ulcer can be selected by the authors themselves.

  d. Rats, mice or guinea pigs were selected for the galactopylorus method. After anesthesia, the skin and muscle layer of the abdominal wall were cut under the xiphoid process from the middle of the abdomen with aseptic technique. The incision length was about 3cm, the stomach was exposed, and the junction of the chingyou portal and duodenum was identified along the stomach to the right. Absolute fasting and no water after surgery. Pyloric ligation can stimulate the secretion of gastric juice and retention of high acidity gastric juice in the stomach, resulting in gastric ulcer. This kind of ulcer replication method is simple, rapid occurrence, high success rate, but the lesion is shallow, strictly speaking, it still belongs to the acute hemorrhagic erosion of gastric mucosa, and the typical lesion of human gastric ulcer is much different, suitable for exploring the research of anti-ulcer drugs and the pathogenesis of gastric ulcer.

  Other ulcers can be caused by surgical removal of alkaline bile, pancreatic or duodenal fluid from the upper part of the intestine, which neutralizes stomach acid. Ulcers can also be caused by stimulation, injury or destruction of brain tissue.

• (4) Pancreatitis model
  Reproducing the pancreatitis model can be used to retain pancreatic fluid exocrine. Activating various pancreatic enzymes in the pancreatic duct system; Infection or the action of certain microbial toxins that affect the nutrition, metabolism, etc., of the pancreas. The experimental animals were dogs, rabbits and rats. The slow injection of dog's own bile into the pancreatic parenchyma at the junction of the body and tail of the pancreas at 0.5ml/kg can cause local necrosis and inflammatory infiltration of the pancreas, which is similar to acute pancreatitis and lesions in humans. Acute pancreatitis can be induced by using E. coli suspension of 900million/ml and 1ml/kg body weight into the pancreatic duct of rabbits. In addition, continuous intraperitoneal injection of ethylthiamine can also induce successful pancreatitis in rats. With the prolongation of injection time of ethylthiamine, extensive progressive destruction and degeneration of pancreatic tissue and continuous decline of pancreatic enzyme level can occur.
• (5) Diabetes model
  The diabetic model was replicated by injecting hyperglycemic factors. Surgical removal of all or most of the pancreas; Alloxan was used to destroy pancreatic β cells, resulting in pancreatic diabetes. The injection of phloridin interferes with the reabsorption of sugar by renal tubules and destroys esterase, resulting in the obstruction of glucose phosphorylation and dephosphorylation, resulting in phloridin glycoderma.
  The diabetic animal model of alloxouracil replication is a better method to study human diabetes at present. Its experimental diabetes is similar to human diabetes, and this derivative may be produced when metabolic disorders occur in the body. The exocrine part of the islet is not damaged, and almost all commonly used experimental animals can be used for experimental research. The function of β cells in model islets is not lost, but decreased to different degrees, which is conducive to the study of islet tissue regeneration and functional recovery, and animals can survive for a long time without insulin injection. The modeling dose is 12mg/100g body weight for rats, 150-200mg /kg body weight for rabbits, and about 50-60mg /kg body weight for dogs. The dosage of phloretin in rabbit skin for diabetic model was 0.5% phloretin at 15m/kg body weight and injected subcutaneously. Note that the solution of alloxouracil and phloridin must be prepared for use.

Product Directory

If you are interested in the details of the experiment or the problems that may arise during the experiment and their causes, please contact: BD@ebraincase.com

literature citation

• Kershaw, E.E.; Flier, J.S. Adipose Tissue as an Endocrine Organ. J. Clin. Endocrinol. Metab. 2004, 89, 2548–2556.
• Han, S.; Sun, H.M.; Hwang, K.-C.; Kim, S.-W. Adipose-Derived Stromal Vascular Fraction Cells: Update on Clinical Utility and Efficacy. Crit. Rev. Eukaryot. Gene Expr. 2015, 25, 145–152.
• Romacho, T.; Elsen, M.; Röhrborn, D.; Eckel, J. Adipose tissue and its role in organ crosstalk. Acta Physiol. 2014, 210, 733–753.
• Szydło, B.; Kiczmer, P.; Swi ˛etochowska, E.; Ostrowska, Z. Role of omentin and chemerin in metabolic ´ syndrome and tumor diseases. Post˛epy Hig. Med. Do´swiadczalnej 2016, 70, 844–849.
• Batra, A.; Siegmund, B. The role of visceral fat. Dig. Dis. 2012, 30, 70–74.
• Strong, A.L.; Burow, M.E.; Gimble, J.M.; Bunnell, B.A. Concise Review: The Obesity Cancer Paradigm: Exploration of the Interactions and Crosstalk with Adipose Stem Cells. Stem Cells 2015, 33, 318–326. Int. J. Mol. Sci. 2020, 21, 8308 20 of 34.
• Yehuda-Shnaidman, E.; Schwartz, B. Mechanisms linking obesity, inflammation and altered metabolism to colon carcinogenesis. Obes. Rev. 2012, 13, 1083–1095. 
• Nieman, K.M.; Romero, I.L.; Van Houten, B.; Lengyel, E. Adipose tissue and adipocytes support tumorigenesis and metastasis. Biochim. Biophys. Acta (BBA) Mol. Cell Biol. Lipids 2013, 1831, 1533–1541.
• Sun, X.; Harris, E.N. New aspects of hepatic endothelial cells in physiology and nonalcoholic fatty liver disease. Am. J. Physiol. Physiol. 2020, 318, C1200–C1213.
• Azzu, V.; Vacca, M.; Virtue, S.; Allison, M.; Vidal-Puig, A. Adipose Tissue-Liver Cross Talk in the Control of Whole-BodyMetabolism: Implications in Nonalcoholic Fatty Liver Disease. Gastroenteroloy 2020, 158, 1899–1912.

Related products

Neurological Disease Models-BrainCase

Tumor animal models-anti-tumor-BrainCase

Digestive System Disease Animal Model-Brain Case

Cardiovascular System Disease Animal Models-Brain Case