Objective: To explore the formation mechanism of benign biliary stricture. Methods: A model of trauma of common bile duct was established in 28 dogs and then repaired. The anasomosis tissues were taken on the 1st week...Objective: To explore the formation mechanism of benign biliary stricture. Methods: A model of trauma of common bile duct was established in 28 dogs and then repaired. The anasomosis tissues were taken on the 1st week, 3rd week and the 3rd month, 6th month respectively after operation and examined by using light microscopy and elec-tromicroscopy. Macrophage, TGF-p, and a-SMA were studied immunohistochemically. Results: The mucosal epithelium of common bile duct restored poorly, chronic inflammation lasted for a long time, fibroblasts proliferated actively, extracellular matrix overdeposited; and myofibroblasts functioned actively and existed during the whole healing process. Immunohistochemical test showed a high expression of macrophage, TGF-β1 and a-SMA during healing process lasting a long duration. Macrophages were found in the lamina propria under mucosa, TGF-β1 in the granulation tissue, fibroblasts and endothelial cells of blood vesssels, while a-SMA in the myofiroblasts and smooth muscle tissue. Conclusion: The healing of bile duct is in the mode of overhealing. Myofibroblast is the main cause for contracture of scar and stricture of bile duct. The high expression of macrophage, TGF-β1 and a-SMA is closely related to active proliferation of fibroblasts, extracelluar matrix overdeposition and scar contracture of bile duct.展开更多
In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investi...In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.展开更多
基金Supported by Shaanxi Scientific Fund(2002-K10-G8)
文摘Objective: To explore the formation mechanism of benign biliary stricture. Methods: A model of trauma of common bile duct was established in 28 dogs and then repaired. The anasomosis tissues were taken on the 1st week, 3rd week and the 3rd month, 6th month respectively after operation and examined by using light microscopy and elec-tromicroscopy. Macrophage, TGF-p, and a-SMA were studied immunohistochemically. Results: The mucosal epithelium of common bile duct restored poorly, chronic inflammation lasted for a long time, fibroblasts proliferated actively, extracellular matrix overdeposited; and myofibroblasts functioned actively and existed during the whole healing process. Immunohistochemical test showed a high expression of macrophage, TGF-β1 and a-SMA during healing process lasting a long duration. Macrophages were found in the lamina propria under mucosa, TGF-β1 in the granulation tissue, fibroblasts and endothelial cells of blood vesssels, while a-SMA in the myofiroblasts and smooth muscle tissue. Conclusion: The healing of bile duct is in the mode of overhealing. Myofibroblast is the main cause for contracture of scar and stricture of bile duct. The high expression of macrophage, TGF-β1 and a-SMA is closely related to active proliferation of fibroblasts, extracelluar matrix overdeposition and scar contracture of bile duct.
基金supported by the State Key Program of National Natural Science of China(81230007)
文摘In heart disease, transforming growth factor-β1 （TGF-β1） converts fibroblasts into myofibroblasts, which synthesize and se- crete fibrillar type I and III collagens. The purpose of the present study was to investigate how hydrogen sulfide （HzS） sup- presses TGF-~l-induced differentiation of human cardiac fibroblasts to myofibroblasts. Human cardiac fibroblasts were se- rum-starved in fibroblast medium for 16 h before exposure to TGF-β1 （10 ng mL-1） for 24 h with or without sodium hydrosul- fide （NariS, 100 μmol L-1, 30 min pretreatment） treatment. NariS, an exogenous HzS donor, potently inhibited the prolifera- tion and migration of TGF-β1-induced human cardiac fibroblasts and regulated their cell cycle progression. Furthermore, NariS treatment led to suppression of fibroblast differentiation into myofibroblasts, and reduced the levels of collagen, TGF-β1, and activated Smad3 in TGF-β1-induced human cardiac fibroblasts in vitro. We therefore conclude that H2S sup- presses TGF-β1-stimulated conversion of fibroblasts to myofibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway, as well as by inhibiting the proliferation, migration, and cell cycle progression of human cardiac myofibroblasts. These effects of H2S may play significant roles in cardiac remodeling associated with heart failure.
