动物造模,慢性胰腺炎模型 z-bio 2023-11-20 1050

　　1. Animal modeling materials: Male SD rats, weighing 180-200g; Medication: Dibutyl dichloride.

　　2. Modeling method: SD rats were randomly divided into an experimental group and a control group. DBTC is first dissolved in 100% ethanol and then mixed with glycerol (in a ratio of 1:2:3). Fasted for 12 hours before the experiment, unable to resist water, and underwent intraperitoneal anesthesia with ketamine at a dose of 10mg/kg body weight. The experimental group was injected with DBTC solution 200 through the tail vein μ L (DBTC 8mg/kg), control group injected with 200 μ A mixed solvent of 100% ethanol and glycerol.

　　3. Modeling principle: The rat pancreas has high organ specificity for DBTC concentration. DBTC damages acinar cells and pancreatic duct epithelial cells, inducing pancreatitis, and necrotic cells block the pancreatic duct, leading to pancreatic duct dilation and accelerated chronic pancreatitis. In the later stage of inflammation, the structure of pancreatic lobules is destroyed, leading to widespread interstitial fibrosis.

　　4. Changes after modeling: DBTC injection for 1 day resulted in pancreatic tissue edema and mild dilation of the pancreatic duct; On the 14th day, pancreatic tissue edema worsened, with significant dilation of the pancreatic duct, particularly in the head and body of the pancreas; On the 21st day, pancreatic tissue showed atrophy, with an irregular and rough surface. Light microscopy observation: After 1 day of DBTC injection, the pancreatic tissue showed acute to moderate interstitial edematous pancreatitis with neutrophil infiltration; Within 7 days, inflammation worsened, with widespread infiltration of neutrophils, monocytes, and fibroblasts, swelling of acini, and scattered necrosis of acinar cells; 14 days of extensive inflammatory cell infiltration, accompanied by mild fibrosis, with a small amount of fibrous tissue deposition in the stroma; Over time from 21 to 28 days, fibrosis gradually worsens, with a large amount of fibrous connective tissue visible; After 60 days, the structure of pancreatic lobules was destroyed, acini disappeared, inflammatory cells infiltrated extensively, fibrous tissue proliferated extensively, and interstitial fibrosis was widespread. The control group showed no significant pathological changes throughout the entire observation period.

　　After 1 day of DBTC injection, serum amylase, lipase, and hyaluronic acid significantly increased. At 7 days, serum amylase returned to normal, and at 14 days, serum lipase returned to normal. The concentration of hyaluronic acid remained higher than that of the control group, but fluctuated repeatedly without time dependence.

　　On the 1st and 7th day of DTBC injection, there was no significant difference in the quantitative staining of collagen fibers compared to the control group. Collagen fibers were scattered around the blood vessels and between lobules. On the 14th day, the positive staining area of collagen fibers around the pancreatic duct and between the lobules significantly increased. On the 21st day, as time went on, the collagen fibers gradually expanded from around the blood vessels and between the lobules into the lobules, and the staining deepened. After 60 days, the structure of pancreatic lobules was destroyed and reconstructed, acini disappeared, and interstitial fibers proliferated extensively in a grid like manner. After 14, 21, 28, and 60 days of modeling, the quantitative analysis of collagen in the experimental group was significantly higher than that in the control group (P<0.01).