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Romana Tomaszewska - One of the best experts on this subject based on the ideXlab platform.
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pretreatment with Obestatin reduces the severity of ischemia reperfusion induced acute pancreatitis in rats
European Journal of Pharmacology, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana Tomaszewska, Artur DembinskiAbstract:Abstract 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: 0.5 h before exposure to ischemia, and 3 h 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: Administration of Obestatin inhibits the development of ischemia/reperfusion-induced acute pancreatitis. This observation, taken together with previous findings that Obestatin protects the pancreas against cerulein-induced pancreatitis, indicates that protective effect of Obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis.
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Obestatin accelerates the recovery in the course of ischemia reperfusion induced acute pancreatitis in rats
PLOS ONE, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana TomaszewskaAbstract:Objective Several previous studies have shown that Obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with Obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of Obestatin administration following the onset of experimental acute pancreatitis. Aim The aim of this study was to evaluate the impact of Obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of Obestatin on daily food intake and pancreatic exocrine secretion. Methods Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of Obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula. Results Treatment with Obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of Obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, Obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP. Conclusion Treatment with the exogenous Obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of Obestatin.
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Pretreatment with Obestatin inhibits the development of cerulein-induced pancreatitis
Journal of Physiology and Pharmacology, 2009Co-Authors: Piotr Ceranowicz, Atsukazu Kuwahara, Romana Tomaszewska, Warzecha Z, Artur Dembiński, Jakub Cieszkowski, Marcin Dembiński, Ryszard Sendur, Kusnierz-cabala B, Kato IAbstract:Obestatin is a peptide derived from the proghrelin, a common prohormone for ghrelin and Obestatin. Obestatin, like the ghrelin has been originally extracted from rat stomach, and the stomach seems to be a major source of circulating Obestatin. Previous studies have shown that administration of ghrelin exhibits protective effect in the pancreas, inhibiting the development of acute pancreatitis. Recent study has shown that Obestatin promotes survival of b-cells and pancreatic islets. Aim of the present study was to investigate the influence of Obestatin administration on the development of cerulein-induced pancreatitis. Studies were performed on male Wistar rats. Acute pancreatitis was induced by cerulein given intraperitoneally 5 times at a dose of 50 µg/kg/dose with 1-h intervals. Obestatin was injected twice intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose. In control saline-treated rats, Obestatin was without effect on pancreatic morphology, serum activity of pancreatic enzymes, serum level of pro-inflammatory interleukin-1b or pancreatic cells proliferation. In animals with induction of acute pancreatitis, morphological examination showed that administration of Obestatin decreased pancreatic leukocyte infiltration and vacuolization of acinar cells. These effects were accompanied by reduction in the pancreatitis-evoked increase in serum level of pancreatic digestive enzymes, lipase amylase and poly-C ribonuclease. Obestatin administered at the highest dose of 16 nmo/kg/dose reduced serum activity of these enzymes by 33, 42 and 44%, respectively. Also serum concentration of pro-inflammatory interleukin-1b was decreased by Obestatin in rats with acute pancreatitis; whereas the pancreatitis-evoked decrease in pancreatic blood flow and pancreatic DNA synthesis was partially reversed. Administration of Obestatin reduces the severity of cerulein-induced acute pancreatitis. This effect is related, at least in part, to the improvement of pancreatic blood flow and reduction in pro- inflammatory interleukin-1b release.
Artur Dembinski - One of the best experts on this subject based on the ideXlab platform.
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Obestatin accelerates the healing of acetic acid induced colitis in rats
Oxidative Medicine and Cellular Longevity, 2016Co-Authors: Aleksandra Matuszyk, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Jakub Cieszkowski, Joanna Bonior, Jolanta Jaworek, P C Konturek, Tadeusz Ambrozy, Artur DembinskiAbstract:Obestatin, a 23-amino acid peptide derived from the proghrelin, has been shown to exhibit some protective and therapeutic effects in the gut. The aim of present study was to determine the effect of Obestatin administration on the course of acetic acid-induced colitis in rats. Materials and Methods. Studies have been performed on male Wistar rats. Colitis was induced by a rectal enema with 3.5% acetic acid solution. Obestatin was administered intraperitoneally twice a day at a dose of 8 nmol/kg, starting 24 h after the induction of colitis. Seven or 14 days after the induction of colitis, the healing rate of the colon was evaluated. Results. Treatment with Obestatin after induction of colitis accelerated the healing of colonic wall damage and this effect was associated with a decrease in the colitis-evoked increase in mucosal activity of myeloperoxidase and content of interleukin-1β. Moreover, Obestatin administration significantly reversed the colitis-evoked decrease in mucosal blood flow and DNA synthesis. Conclusion. Administration of exogenous Obestatin exhibits therapeutic effects in the course of acetic acid-induced colitis and this effect is related, at least in part, to the Obestatin-evoked anti-inflammatory effect, an improvement of local blood flow, and an increase in cell proliferation in colonic mucosa.
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pretreatment with Obestatin reduces the severity of ischemia reperfusion induced acute pancreatitis in rats
European Journal of Pharmacology, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana Tomaszewska, Artur DembinskiAbstract:Abstract 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: 0.5 h before exposure to ischemia, and 3 h 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: Administration of Obestatin inhibits the development of ischemia/reperfusion-induced acute pancreatitis. This observation, taken together with previous findings that Obestatin protects the pancreas against cerulein-induced pancreatitis, indicates that protective effect of Obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis.
Jakub Bukowczan - One of the best experts on this subject based on the ideXlab platform.
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pretreatment with Obestatin reduces the severity of ischemia reperfusion induced acute pancreatitis in rats
European Journal of Pharmacology, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana Tomaszewska, Artur DembinskiAbstract:Abstract 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: 0.5 h before exposure to ischemia, and 3 h 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: Administration of Obestatin inhibits the development of ischemia/reperfusion-induced acute pancreatitis. This observation, taken together with previous findings that Obestatin protects the pancreas against cerulein-induced pancreatitis, indicates that protective effect of Obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis.
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Obestatin accelerates the recovery in the course of ischemia reperfusion induced acute pancreatitis in rats
PLOS ONE, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana TomaszewskaAbstract:Objective Several previous studies have shown that Obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with Obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of Obestatin administration following the onset of experimental acute pancreatitis. Aim The aim of this study was to evaluate the impact of Obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of Obestatin on daily food intake and pancreatic exocrine secretion. Methods Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of Obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula. Results Treatment with Obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of Obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, Obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP. Conclusion Treatment with the exogenous Obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of Obestatin.
Beata Kuśnierzcabala - One of the best experts on this subject based on the ideXlab platform.
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Obestatin accelerates the healing of acetic acid induced colitis in rats
Oxidative Medicine and Cellular Longevity, 2016Co-Authors: Aleksandra Matuszyk, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Jakub Cieszkowski, Joanna Bonior, Jolanta Jaworek, P C Konturek, Tadeusz Ambrozy, Artur DembinskiAbstract:Obestatin, a 23-amino acid peptide derived from the proghrelin, has been shown to exhibit some protective and therapeutic effects in the gut. The aim of present study was to determine the effect of Obestatin administration on the course of acetic acid-induced colitis in rats. Materials and Methods. Studies have been performed on male Wistar rats. Colitis was induced by a rectal enema with 3.5% acetic acid solution. Obestatin was administered intraperitoneally twice a day at a dose of 8 nmol/kg, starting 24 h after the induction of colitis. Seven or 14 days after the induction of colitis, the healing rate of the colon was evaluated. Results. Treatment with Obestatin after induction of colitis accelerated the healing of colonic wall damage and this effect was associated with a decrease in the colitis-evoked increase in mucosal activity of myeloperoxidase and content of interleukin-1β. Moreover, Obestatin administration significantly reversed the colitis-evoked decrease in mucosal blood flow and DNA synthesis. Conclusion. Administration of exogenous Obestatin exhibits therapeutic effects in the course of acetic acid-induced colitis and this effect is related, at least in part, to the Obestatin-evoked anti-inflammatory effect, an improvement of local blood flow, and an increase in cell proliferation in colonic mucosa.
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pretreatment with Obestatin reduces the severity of ischemia reperfusion induced acute pancreatitis in rats
European Journal of Pharmacology, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana Tomaszewska, Artur DembinskiAbstract:Abstract 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: 0.5 h before exposure to ischemia, and 3 h 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: Administration of Obestatin inhibits the development of ischemia/reperfusion-induced acute pancreatitis. This observation, taken together with previous findings that Obestatin protects the pancreas against cerulein-induced pancreatitis, indicates that protective effect of Obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis.
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Obestatin accelerates the recovery in the course of ischemia reperfusion induced acute pancreatitis in rats
PLOS ONE, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana TomaszewskaAbstract:Objective Several previous studies have shown that Obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with Obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of Obestatin administration following the onset of experimental acute pancreatitis. Aim The aim of this study was to evaluate the impact of Obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of Obestatin on daily food intake and pancreatic exocrine secretion. Methods Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of Obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula. Results Treatment with Obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of Obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, Obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP. Conclusion Treatment with the exogenous Obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of Obestatin.
Zygmunt Warzecha - One of the best experts on this subject based on the ideXlab platform.
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Obestatin accelerates the healing of acetic acid induced colitis in rats
Oxidative Medicine and Cellular Longevity, 2016Co-Authors: Aleksandra Matuszyk, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Jakub Cieszkowski, Joanna Bonior, Jolanta Jaworek, P C Konturek, Tadeusz Ambrozy, Artur DembinskiAbstract:Obestatin, a 23-amino acid peptide derived from the proghrelin, has been shown to exhibit some protective and therapeutic effects in the gut. The aim of present study was to determine the effect of Obestatin administration on the course of acetic acid-induced colitis in rats. Materials and Methods. Studies have been performed on male Wistar rats. Colitis was induced by a rectal enema with 3.5% acetic acid solution. Obestatin was administered intraperitoneally twice a day at a dose of 8 nmol/kg, starting 24 h after the induction of colitis. Seven or 14 days after the induction of colitis, the healing rate of the colon was evaluated. Results. Treatment with Obestatin after induction of colitis accelerated the healing of colonic wall damage and this effect was associated with a decrease in the colitis-evoked increase in mucosal activity of myeloperoxidase and content of interleukin-1β. Moreover, Obestatin administration significantly reversed the colitis-evoked decrease in mucosal blood flow and DNA synthesis. Conclusion. Administration of exogenous Obestatin exhibits therapeutic effects in the course of acetic acid-induced colitis and this effect is related, at least in part, to the Obestatin-evoked anti-inflammatory effect, an improvement of local blood flow, and an increase in cell proliferation in colonic mucosa.
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pretreatment with Obestatin reduces the severity of ischemia reperfusion induced acute pancreatitis in rats
European Journal of Pharmacology, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana Tomaszewska, Artur DembinskiAbstract:Abstract 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: 0.5 h before exposure to ischemia, and 3 h 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: Administration of Obestatin inhibits the development of ischemia/reperfusion-induced acute pancreatitis. This observation, taken together with previous findings that Obestatin protects the pancreas against cerulein-induced pancreatitis, indicates that protective effect of Obestatin in the pancreas is universal and independent of the primary cause of acute pancreatitis.
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Obestatin accelerates the recovery in the course of ischemia reperfusion induced acute pancreatitis in rats
PLOS ONE, 2015Co-Authors: Jakub Bukowczan, Zygmunt Warzecha, Piotr Ceranowicz, Beata Kuśnierzcabala, Romana TomaszewskaAbstract:Objective Several previous studies have shown that Obestatin exhibits protective and regenerative effects in some organs including the stomach, kidney, and the brain. In the pancreas, pretreatment with Obestatin inhibits the development of cerulein-induced acute pancreatitis, and promotes survival of pancreatic beta cells and human islets. However, no studies investigated the effect of Obestatin administration following the onset of experimental acute pancreatitis. Aim The aim of this study was to evaluate the impact of Obestatin therapy in the course of ischemia/reperfusion-induced pancreatitis. Moreover, we tested the influence of ischemia/reperfusion-induced acute pancreatitis and administration of Obestatin on daily food intake and pancreatic exocrine secretion. Methods Acute pancreatitis was induced by pancreatic ischemia followed by reperfusion of the pancreas. Obestatin (8nmol/kg/dose) was administered intraperitoneally twice a day, starting 24 hours after the beginning of reperfusion. The effect of Obestatin in the course of necrotizing pancreatitis was assessed between 2 and 14 days, and included histological, functional, and biochemical analyses. Secretory studies were performed on the third day after sham-operation or induction of acute pancreatitis in conscious rats equipped with chronic pancreatic fistula. Results Treatment with Obestatin ameliorated morphological signs of pancreatic damage including edema, vacuolization of acinar cells, hemorrhages, acinar necrosis, and leukocyte infiltration of the gland, and led to earlier pancreatic regeneration. Structural changes were accompanied by biochemical and functional improvements manifested by accelerated normalization of interleukin-1β level and activity of myeloperoxidase and lipase, attenuation of the decrease in pancreatic DNA synthesis, and by an improvement of pancreatic blood flow. Induction of acute pancreatitis by pancreatic ischemia followed by reperfusion significantly decreased daily food intake and pancreatic exocrine secretion. Administration of Obestatin at doses used was without significant effect with regard to daily food intake or pancreatic exocrine secretion in sham-operated rats, as well as in rats with acute pancreatitis. On the other hand, Obestatin abolished a statistical significance of difference in food intake between animals with AP and control animals without pancreatic fistula and induction of AP. Conclusion Treatment with the exogenous Obestatin reduces severity of ischemia/reperfusion-induced acute pancreatitis and accelerates recovery in this disease. The involved mechanisms are likely to be multifactorial, and are mediated, at least in part, by anti-inflammatory properties of Obestatin.