title: Cell cycle characteristics of the pancreas in an animal model of isolated pancreatic trauma.
abstract: BACKGROUND
  In our previous study, we established a small animal model that mimicked the pathophysiology of isolated pancreatic trauma. To gain further insights into the relationships between tissue damage and the ability of the pancreatic cells to regenerate, we induced pancreatic trauma in rats maintained over 7 days and analyzed both the alteration of the cell death and the cell cycle distribution of the pancreatic cells in this study.
  
  
  METHODS
  The rats were divided into two groups as follows: impact and control. The pancreas in the impact group was injured by a BIM-III biotical impact machine. Pancreatic enzyme activity, the level of Ca in the serum, pancreatic cell death, and cell cycle characteristics were examined after the trauma.
  
  
  RESULTS
  In the impact groups, lipase was activated later than amylase and lasted persistently. The levels of serum Ca decreased at 6 hours after injury, sharply declined at 24 hours and 72 hours compared with the control groups, and returned to normal levels at 7 days. The pancreatic trauma also induced the compensatory proliferation of pancreatic cells. The results from a TUNEL stain, flow cytometry, Western blot, and immunohistochemistry indicated that pancreatic trauma induces cell death and the compensatory proliferation of pancreatic cells.
  
  
  CONCLUSIONS
  Detecting amylase and lipase at the same time can help us determine the exocrine function of pancreas. Serum Ca can be used as an indicator for estimating the severity of pancreatic trauma. The cell cycle characteristics of the pancreas in the animal model of isolated pancreatic trauma indicate that the proper remedial time is in the first 24 hours after the pancreatic trauma.
authors.affiliation: From the General Surgery Center (D.R.-W., C.G.-Y., H.Z., Y.H.-T., L.H.-Y., W.T., L.N., T.L.-J.), and Cadre's Ward (H.F.-Q.), Chengdu Military General Hospital, Chengdu; and Institute of Organ Transplantation (C.L.-P.), The 309th Hospital of Chinese People's Liberation Army, Beijing, China.
authors.forename: Dai
authors.initials: D
authors.lastname: Rui-Wu
authors.forename: Chen
authors.initials: C
authors.lastname: Guang-Yu
authors.forename: He
authors.initials: H
authors.lastname: Fa-Qun
authors.forename: Huang
authors.initials: H
authors.lastname: Zu
authors.forename: Yan
authors.initials: Y
authors.lastname: Hong-Tao
authors.forename: Liang
authors.initials: L
authors.lastname: Hong-Yin
authors.forename: Wang
authors.initials: W
authors.lastname: Tao
authors.forename: Lin
authors.initials: L
authors.lastname: Ning
authors.forename: Tang
authors.initials: T
authors.lastname: Li-Jun
authors.forename: Chen
authors.initials: C
authors.lastname: Li-Ping
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D002118:Calcium / Q000097:blood; D002453:Cell Cycle / Q000502:physiology*; D004195:Disease Models, Animal; D005434:Flow Cytometry; D020287:In Situ Nick-End Labeling; D008049:Lipase / Q000097:blood; D008297:Male; D010179:Pancreas / Q000166:cytology / Q000293:injuries* / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration / Q000502:physiology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D008049:Lipase; D000681:Amylases; D002118:Calcium