November 12, 2014
Notes: Aimoto, Takayuki
J Nippon Med Sch. 2013;80(2):148-54.
Author Address: Department of Surgery, Nippon Medical School, Tokyo, Japan. firstname.lastname@example.org
Reference Type: Journal Article
Record Number: 5218Author: Akyazi, I., Eraslan, E., Gulcubuk, A., Ekiz, E. E., Cirakli, Z. L., Haktanir, D., Bala, D. A., Ozkurt, M., Matur, E. and Ozcan, M.
Title: Long-term aspirin pretreatment in the prevention of cerulein-induced acute pancreatitis in rats
Journal: World J Gastroenterol
Date: May 21
Short Title: Long-term aspirin pretreatment in the prevention of cerulein-induced acute pancreatitis in rats
Alternate Journal: World journal of gastroenterology : WJG
ISSN: 2219-2840 (Electronic)
Accession Number: 23704822
Anti-Inflammatory Agents, Non-Steroidal/*administration & dosage
Aspirin/*administration & dosage
Disease Models, Animal
Drug Administration Schedule
Lipid Peroxidation/drug effects
Oxidative Stress/drug effects
Pancreatitis/blood/chemically induced/pathology/*prevention & control
Abstract: AIM: To investigate the effects of long term pretreatment with low-, medium- and high-dose aspirin (acetylsalicylic acid, ASA) on a model of acute pancreatitis (AP) induced in rats. METHODS: Forty male Wistar rats were used. Three experimental groups, each consisting of eight animals, received low- (5 mg/kg per day), medium- (150 mg/kg per day) and high-dose (350 mg/kg per day) ASA in supplemented pellet chow for 100 d. Eight animals, serving as the AP-control group, and another eight, serving as reference value (RV) group, were fed with standard pellet chow for the same period. After pretreatment, AP was induced in the experimental animals by intraperitoneal administration of cerulein (2 x 50 mug/kg), while the RV group received saline in the same way. Twelve hours after the second injection, the animals were sacrificed. Pancreatic tissue and plasma samples were collected. One part of the collected pancreatic tissues was used for histopathological evaluation, and the remaining portion was homogenized. Cytokine levels [tumor necrosis factor, interleukin (IL)-1beta, IL-6], hemogram parameters, biochemical parameters (amylase and lipase), nuclear factor-kappaB, aspirin triggered lipoxins and parameters related to the antioxidant system (malondialdehyde, nitric oxide, hemeoxygenase-1, catalase and superoxide dismutase) were measured. RESULTS: Cerulein administration induced mild pancreatitis, characterized by interstitial edema (total histopathological score of 5.88 +/- 0.44 vs 0.25 +/- 0.16, P < 0.001). Subsequent pancreatic tissue damage resulted in an increase in amylase (2829.71 +/- 772.48 vs 984.57 +/- 49.22 U/L, P = 0.001) and lipase (110.14 +/- 75.84 U/L vs 4.71 +/- 0.78 U/L, P < 0.001) in plasma, and leucocytes (6.89 +/- 0.48 vs 4.36 +/- 0.23, P = 0.001) in peripheral blood. Cytokines, IL-1beta (18.81 +/- 2.55 pg/mug vs 6.65 +/- 0.24 pg/mug, P = 0.002) and IL-6 (14.62 +/- 1.98 pg/mug vs 9.09 +/- 1.36 pg/mug, P = 0.04) in pancreatic tissue also increased. Aspirin pretreatment reduced the increase in the aforementioned parameters to a certain degree and partially improved the histopathological alterations caused by cerulein. No evidence of side effects related to chronic ASA administration (e.g., inflammation or bleeding) was observed in the gastrointestinal tract in macroscopic and histopathological examination. CONCLUSION: Long term ASA pretreatment could prevent and/or ameliorate certain hematological, serological and histological alterations caused by cerulein-induced AP.