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您的检索式：作者名="Susanne Netter"
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| 1 | Heme oxygenase-1 overexpression increases liver injury after bile duct ligation in rats显示文摘AIM: To investigate the effects of heme oxygenase-1 (HO-1) against oxidant-induced injury caused by bile duct ligation (BDL). METHODS: Either cobalt protoporphyrin (CoPP), a HO-1 inducer, or saline were injected intraperitoneally in male SD-rats. Three days later, BDL or sham-operations were performed. Rats were sacrificed 3 wk after BDL and livers were harvested for histology. Fibrosis was evaluated by sirius red staining and image analysis. Alpha-smooth muscular actin, which indicates activation of stellate cells, was detected by immunohistochemical staining, and cytokine and collagen-Ⅰα (Col-Ⅰα) mRNA expression was detected using RNase protection assays. RESULTS: Serum alanine transaminase increased 8-fold above normal levels one day after BDL. Surprisingly, enzyme release was not reduced in rats receiving CoPP. Liver fibrosis was evaluated 3 wk after BDL and the sirius red-positive area was found to be increased to about 7.8%. However, in CoPP pretreated rats sirius red- positive areas were increased to about 11.7% after BDL. Collagen-Ⅰα and TGF-β mRNA increased significantly by BDL. Again, this effect was increased by HO-1 overexpression.CONCLUSION: Hepatic fibrosis due to BDL is not reduced by the HO-1 inducer CoPP. In contrast, HO-1 overexpression increases liver injury in rats under conditions of experimental chronic cholestasis. | Matthias Froh Lars Conzelmann Peter Walbrun Susanne Netter Reiner Wiest Michael D Wheeler Mark Lehnert Takehiko Uesugi Jurgen Scholmerich Ronald G Thurman | 2007 | World Journal of Gastroenterology2007，13，25： | 4 |
| 2 | Dietary glycine blunts liver injury after bile duct ligation in rats显示文摘AIM: To investigate the effects of (dietary) glycine against oxidant-induced injury caused by bile duct ligation (BDL). METHODS: Either a diet containing 5% glycine or a standard diet was fed to male Sprague-Dawley (SD) rats. Three days later,BDL or sham-operation was performed. Rats were sacrificed 1 to 3 d after BDL. The influence of deoxycholic acid (DCA) in the presence or absence of glycine on liver cells was determined by measurement of calcium and chloride influx in cultivated Kupffer cells and lactate dehydrogenase (LDH) activity was determined in the supernatant of cultivated hepatocytes. RESULTS: Serum alanine transaminase levels increased to about 600 U/L 1 d after BDL. However,enzyme release was blunted by about two third in rats receiving glycine. Release of the alkaline phosphatase and aspartate aminotransferase was also blocked significantly in the group fed glycine. Focal necrosis was observed 2 d after BDL. Glycine partially blocked the histopathological changes. Incubation of Kupffer cells with DCA led to increased intracellular calcium that could be blocked by incubation with glycine. However,systemic blockage of Kupffer cells with gadolinium chloride had no effects on transaminase release. Incubation of isolated hepatocytes with DCA led to a significant release of LDH after 4 h. This release was largely blocked when incubation with glycine was performed. CONCLUSION: These data indicate that glycine significantly decreased liver injury,most likely by a direct effect on hepatocytes. Kupffer cells do not appear to play an important role in the pathological changes caused by cholestasis. | Matthias Froh Zhi Zhong Peter Walbrun Mark Lehnert Susanne Netter Reiner Wiest Lars Conzelmann Erwin Gabele Claus Hellerbrand Jurgen Scholmerich Ronald G Thurman | 2008 | World Journal of Gastroenterology2008，14，39： | 0 |
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