Obestatin, as
ghrelin, has been originally extracted from the stomach, which remains its major source. Previous studies have shown that administration of
obestatin exhibits protective and healing-promoting effects in several organs, including the stomach and kidney. In pancreas, pretreatment with
obestatin inhibits the development of
cerulein-induced
acute pancreatitis and promotes survival of pancreatic beta cells and human islets. The aim of the present study was to check the universality of protective effect of
obestatin in the pancreas. For this reason we investigated the influence of
obestatin administration on the development of
ischemia/reperfusion-induced
pancreatitis.
Acute pancreatitis was induced by pancreatic
ischemia followed by reperfusion of the gland.
Obestatin (4, 8 or 16 nmol/kg/dose) was administered intraperitoneally twice: 0.5h before exposure to
ischemia, and 3h after the first injection. The effect of
obestatin on the course of necrotizing
pancreatitis was assessed after 6-h reperfusion, and included histological, functional, and biochemical analyses. Treatment with
obestatin reduced morphological signs of pancreatic damage including
edema, vacuolization of acinar cells,
hemorrhages, acinar
necrosis, and leukocyte infiltration of the gland. These effects were accompanied by an improvement of pancreatic
DNA synthesis and
superoxide dismutase activity, and a decrease in serum level of
lipase and pro-inflammatory interleukin-1β. Moreover pretreatment with
obestatin reduced
myeloperoxidase activity and
malondialdehyde concentration in pancreatic tissue of rats with
acute pancreatitis.
CONCLUSIONS: