The role of mast cells in the inflammation and fibrosis of the trinitrobenzene sulfonic acid-induced rat pancreatic fibrosis
- VernacularTitle:肥大细胞在大鼠胰腺组织纤维化形成中的作用及其机制
- Author:
Bojing LI
;
Xingpeng WANG
;
Kai WU
- Publication Type:Journal Article
- Keywords:
Pancreatic fibrosis;
Mast cells;
Trinitrobenenze sulfonic acid;
Pancreatic stellate cell;
Angiotensin II receptor
- From:
Chinese Journal of Digestion
2001;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
Objectives To analyze the role and mechanisms of mast cells in the inflammation and fibrosis of 2 ,4, 6-trinitrobenzene sulfonic acid (TNBS)-induced rat pancreatic fibrosis. Methods Rats were received the aseptic instillation of TNBS in ethanol via bilo-pancreatic duct, and then injected with nedocromil sodium, a mast cell stabilizer, and compound 18/80, a mast cell activator, or saline. Rats were sacrificed respectively on 3, 7, 14, 21 or 28 days. Pancreatic inflammation and fibrosis were assessed by gross and histopathological evaluation. Pancreatic fibrosis were observed by Van Gieson. Pancreatic mast cells distribution, number and their state of activation (toluidine blue) were evaluated. The activation of pancreatic stellate cells (PSCs) were assessed by the expression of a-smooth muscle actin (?-SMA) through immunohistochemistry. The expression of angiotensin Ⅱ AT1 and AT2 receptors and transforming growth factor (TGF) ? 1 raRNA, which were the factors of fibrogenesis, were also assessed. Results Typical pancreatic fibrosis changes occurred in the model of rats received TNBS at 4th week by morphological evaluation. The positive expression of ?-SMA and TGF?1 in the pancreatic tissues were detected at day 3, especially at 4th week. The expression of angiotensin Ⅱ AT1 and AT2 receptors mRNA increased gradually in all the three groups, also especially at 4th week. Compared to the control group, there were more higher expression of ?-SMA, TGF?1, angiotensin Ⅱ AT1 and AT2 receptor in the compound 48/80 group, while there were lower expression of these proteins in the nedocromil group. Conclusions Mast cells are involved in TNBS-induced pancreatic inflammation and fibrosis in rats. After being activated, mast cells will promote the activation and proliferation of PSCs and upregulate the expression of angiotensin Ⅱ AT1 receptor and AT2 receptor, and then lead to pancreatic fibrosis gradually.
