Mediating effects of mast cells on the progression of pancreatic fibrogenesis in rats with chronic pancreatitis
Wang Xingpen
Abstract
Wang Xingpen
Abstract
Objective To investigate the number and distribution of mast cells (MCs) and their potential role in the progression of trinitrobenenze sulfonic acid (TNBS) induced pancreatic fibrosis in rats. Methods The rat pancreatic fibrosis model was established by infusion of 2% TNBS ethyl alcohol solution into the cholangiopancreatic duct. The animals were sacrificed on day 3, week 1 and 4 after operation. The pathologic changes and the extent of fibrosis of the pancreas were studied by H E staining. MCs in the pancreas were stained by thionine blue, and activation of PSCs, which was indicated by measurement of α SMA, was determined by immunochemistry. Results Inflammation was the major histopathologic change in the pancreas after injection of TNBS solution and interstitial fibrosis was increasingly noted later. On day 3, the number of MCs was increased, mainly localized in the interstitial of the pancreas. At week 1, the number of MCs increased significantly ( P 0.05 vs 3 d ), and the MCs distributed predominantly in the fibrotic area. At 4 week, the number of MCs increased significantly ( P 0.01 vs 1 week), and the percentage of degranulation was also increased in the fibrotic area, but in the other area the number and distribution of MCs remained unchanged ( P 0 05 vs 3 d). The staining of α SMA of PSCs was mildly positive at 3 d, but the positivity became more evident after 1 week, mainly in the fibrous area and the pancreatic duct. The expression of α SMA of PSCs in the normal area was dispersed. Conclusions Activation of MCs might play a mediating regulatory role in the progress of pancreatic fibrosis through degranulation. This action is possibly related to the release of cytokines, which stimulate the activation of PSCs.
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Objective To investigate the number and distribution of mast cells (MCs) and their potential role in the progression of trinitrobenenze sulfonic acid (TNBS) induced pancreatic fibrosis in rats. Methods The rat pancreatic fibrosis model was established by infusion of 2% TNBS ethyl alcohol solution into the cholangiopancreatic duct. The animals were sacrificed on day 3, week 1 and 4 after operation. The pathologic changes and the extent of fibrosis of the pancreas were studied by H E staining. MCs in the pancreas were stained by thionine blue, and activation of PSCs, which was indicated by measurement of α SMA, was determined by immunochemistry. Results Inflammation was the major histopathologic change in the pancreas after injection of TNBS solution and interstitial fibrosis was increasingly noted later. On day 3, the number of MCs was increased, mainly localized in the interstitial of the pancreas. At week 1, the number of MCs increased significantly ( P 0.05 vs 3 d ), and the MCs distributed predominantly in the fibrotic area. At 4 week, the number of MCs increased significantly ( P 0.01 vs 1 week), and the percentage of degranulation was also increased in the fibrotic area, but in the other area the number and distribution of MCs remained unchanged ( P 0 05 vs 3 d). The staining of α SMA of PSCs was mildly positive at 3 d, but the positivity became more evident after 1 week, mainly in the fibrous area and the pancreatic duct. The expression of α SMA of PSCs in the normal area was dispersed. Conclusions Activation of MCs might play a mediating regulatory role in the progress of pancreatic fibrosis through degranulation. This action is possibly related to the release of cytokines, which stimulate the activation of PSCs.
Key concepts: Pancreatitis, Pancreas, Fibrosis, Pancreatic duct, Medicine, Staining, Degranulation, Pathology