作者: Raghuwansh P Sah , Vikas Dudeja , Rajinder K Dawra , Ashok K Saluja , None
DOI: 10.1053/J.GASTRO.2013.01.041
关键词:
摘要: Background & Aims Premature activation of trypsinogen can cause pancreatic injury and has been associated with chronic pancreatitis (CP). Mice that lack intra-acinar trypsinogen, such as trypsinogen-7−null ( T -/- ) cathepsin B–null CB mice, have used to study trypsin-independent processes CP development. We compared histologic features inflammatory responses tissues from these mice those wild-type after the development CP. Methods was induced in wild-type, , by twice-weekly induction acute for 10 weeks; hourly intraperitoneal injections cerulein (50 μg/kg × 6). Pancreatic samples were collected evaluated immunohistochemical analyses. Normal human pancreas samples, obtained islet transplant program at University Minnesota, controls surgical resections. Results Compared had similar levels atrophy, histomorphologic CP, inflammation. All comparable nuclear factor (NF)-κB, a transcription regulates response, immediately injection cerulein. tissue patients increased NF-κB (based on translocation p65 acinar cells) controls. Conclusions Induction does not require trypsinogen. cells controls; regulation response this might be involved pathogenesis