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Acetyl‐ l ‐Carnitine Ameliorates Caerulein‐induced Acute Pancreatitis in Rats
Author(s) -
Arafa Hossam M. M.,
Hemeida Ramadan A. M.,
Hassan Mohamed I. A.,
AbdelWahab Mohammed H.,
Badary Osama A.,
Hamada Farid M. A.
Publication year - 2009
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2009.00399.x
Subject(s) - acute pancreatitis , pancreatitis , medicine , nitric oxide , endocrinology , myeloperoxidase , glutathione , pancreatic injury , carnitine , malondialdehyde , pancreatic disease , pancreas , inflammation , chemistry , enzyme , oxidative stress , biochemistry
In the present study, we have addressed the possible protective role of acetyl‐ l ‐carnitine in caerulein‐induced acute pancreatitis in male Swiss albino rats. Acute pancreatitis paradigm was developed by challenging animals with a supramaximal dose of caerulein (20 µg/kg, SC) four times at hourly intervals. Caerulein induced acute pancreatitis that was well‐characterized morphologically and biochemically. Severe oedema with marked increased relative pancreatic weight, marked atrophy of acini with increased interacinar spaces, vacuolization, and extensive leucocytic infiltration were diagnostic fingerprints of the pancreatitis phenotype. A biochemical test battery that confirmed the model comprised increased plasma amylase and lipase activities, calcium levels as well as increased pancreatic enzymatic myeloperoxidase and glutathione‐ S ‐transferase activities, beside increased pancreatic contents of nitric oxide and malondialdehyde and reduced pancreatic glutathione level. Prior administration of acetyl‐ l ‐carnitine (200 mg/kg, IP) for seven consecutive days ahead of caerulein challenge alleviated all the histological and biochemical manifestations of acute pancreatitis. These results suggest a possible protective role of the carnitine ester in such a murine acute pancreatitis model probably via regulation of the oxidant/antioxidant balance, beside modulation of the myeloperoxidase and nitric oxide systems, which are involved in the inflammatory cascade that most often associate the disease.