Histological study of the protective effect of N-acetylcysteine on pancreatic acinar cells in experimentally induced acute pancreatitis in male albino rats

ABSTRACT

Despite extensive research efforts, there is a lack of specific medical/ pharmacological interventions of excellent clinical value in acute pancreatitis. The exact mechanisms by which diverse etiological factors induce an attack are unclear. Since reactive oxygen species [OR] are involved in acute pancreatitis, the present study was designed to assess the protective role of N-acetylcysteine in preventing the histological changes in pancreatic acinar cells, induced by L-arginine in albino rats. Twenty five male albino rats weighing 250-300g were included in this study. They were divided into four groups. Group I [10 rats] the control group was further divided into Group Ia 5 animals received physiological saline injections i.p. Group Ib 5 animals received N-acetylcysteine in a single dose of 50 mg/kg orally. Group II [5 rats] in the treated group, acute pancreatitis was induced by two injections of 250 mg/100 g body weight of L-Arginine intraperitoneally in an 1-h interval. Group III [5 rats] the animals were administered N-acetylcysteine in the same dose as that given to group Ib 1 hour prior to L-Arg administration. Group IV [5 rats] the rats received the same dose of N-acetylcysteine 1h after L-Arg was given. All rats were sacrificed 24 h after the second L-Arg injection. Specimens from the pancreas of each animal were subjected to light microscopic examination using Haematoxylin and Eosin stain and ultrastructural examination. Histological results of group II [rats received L-Arginine] showed variable histological changes with different severity. Interlobular and interstitial tissue oedema, cellular infiltration and extravasation of blood appered in some sections. The peripheral fat cells were necrotic. Most lobules revealed loss of normal architecture with focal peripheral areas of acinar cell lysis. Some acinar cells showed cytoplasmic vacuolations and nuclear changes. Marked dilatation of rER, focal areas of rarefaction and depletion of zymogen granules were also noticed in ultrastructural examination. Pretreatment with N-acetylcysteine revealed marked protective effect on the histological changes of pancreatitis induced by L-arginine. This protection was less evident in group IV receiving N-acetylcysteine after administration of L-arginine and induction of pancreatitis. N-acetylcysteine proved to be of benefit in protection of the pancreas from the experimentally induced pancreatitis by L-arginine especially if administered before induction. Supplemental antioxidant therapy seems promising in the regulation of the progress of acute pancreatitis and it is recommended to be given to patients at an earlier stage or those at risk for the development of acute pancreatitis