OBJECTIVE: The aims of this study were to clarify the kinetics of intestinal barrier function impairment in sodium taurocholate-induced severe acute pancreatitis (SAP) models and to explore an appropriate concentration of sodium taurocholate and a suitable time point for further study. METHODS: In total, 104 rats were randomly divided into four groups: the normal control group (n = 8) receiving no treatment, the sham-operation group (n = 32), the 2.5% and 5% sodium taurocholate-treated SAP groups (n = 32 for each group) which were induced via a retrograde injection of 2.5% or 5% sodium taurocholate into the pancreatic duct. Histological examination, serum D-lactate and endotoxin levels and the incidence of bacteria translocation were recorded to assess the intestinal mucosal injury. RESULTS: Pancreatitis models were successfully established in both the 2.5% and 5% sodium taurocholate-treated groups. The dosage of sodium taurocholate used to induce pancreatitis was positively correlated with the degree of intestinal mucosal injury. The most severe damage to intestinal barrier was observed 24 h after surgery in the 2.5% sodium taurocholate-treated group and 48 h after surgery in the 5% sodium taurocholate-treated group, respectively. CONCLUSION: Based on the success rate of the model, the mortality and the impairment of intestinal barrier function, we conclude that 24 h after a retrograde injection of 2.5% sodium taurocholate may be the most appropriate time point to study intestinal barrier injury in SAP rats.
OBJECTIVE: The aims of this study were to clarify the kinetics of intestinal barrier function impairment in sodium taurocholate-induced severe acute pancreatitis (SAP) models and to explore an appropriate concentration of sodium taurocholate and a suitable time point for further study. METHODS: In total, 104 rats were randomly divided into four groups: the normal control group (n = 8) receiving no treatment, the sham-operation group (n = 32), the 2.5% and 5% sodium taurocholate-treated SAP groups (n = 32 for each group) which were induced via a retrograde injection of 2.5% or 5% sodium taurocholate into the pancreatic duct. Histological examination, serum D-lactate and endotoxin levels and the incidence of bacteria translocation were recorded to assess the intestinal mucosal injury. RESULTS:Pancreatitis models were successfully established in both the 2.5% and 5% sodium taurocholate-treated groups. The dosage of sodium taurocholate used to induce pancreatitis was positively correlated with the degree of intestinal mucosal injury. The most severe damage to intestinal barrier was observed 24 h after surgery in the 2.5% sodium taurocholate-treated group and 48 h after surgery in the 5% sodium taurocholate-treated group, respectively. CONCLUSION: Based on the success rate of the model, the mortality and the impairment of intestinal barrier function, we conclude that 24 h after a retrograde injection of 2.5% sodium taurocholate may be the most appropriate time point to study intestinal barrier injury in SAP rats.
Authors: Glen M DeLoid; Yanli Wang; Klara Kapronezai; Laura Rubio Lorente; Roujie Zhang; Georgios Pyrgiotakis; Nagarjun V Konduru; Maria Ericsson; Jason C White; Roberto De La Torre-Roche; Hang Xiao; David Julian McClements; Philip Demokritou Journal: Part Fibre Toxicol Date: 2017-10-13 Impact factor: 9.400
Authors: Fons F van den Berg; Demi van Dalen; Sanjiv K Hyoju; Hjalmar C van Santvoort; Marc G Besselink; Willem Joost Wiersinga; Olga Zaborina; Marja A Boermeester; John Alverdy Journal: Gut Date: 2020-09-01 Impact factor: 23.059