Limits...
Administration of obestatin accelerates the healing of chronic gastric ulcers in rats.

Dembiński A, Warzecha Z, Ceranowicz P, Cieszkowski J, Dembiński M, Ptak-Belowska A, Kuwahara A, Kato I - Med. Sci. Monit. (2011)

Bottom Line: Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis.These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Jagiellonian University Medical College, Cracow, Poland. mpdembin@cyf-kr.edu.pl

ABSTRACT

Background: Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis. The aim of the present study was to investigate the influence of obestatin administration on the healing of chronic gastric ulcers.

Material/methods: Chronic gastric ulcers were induced in rats by 100% acetic acid applied to the serosal surface of the gastric wall. Obestatin was given twice a day intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose for 6 days. Six days after induction of ulcers, rats were anesthetized and the stomach was exposed for measurement of gastric blood flow and ulcer area. Biopsy samples from the gastric mucosa were taken for determination of mucosal DNA synthesis and for measurement of gastric expression of mRNA for interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).

Results: Induction of gastric ulcers alone increased mucosal blood flow and tissue expression of mRNA for TNF-alpha and IL-1beta, whereas gastric mucosal DNA synthesis was reduced. In rats with gastric ulcers, administration of obestatin increased gastric mucosal blood flow, accelerated the healing rate of these ulcers and partly reversed the gastric ulcer-induced reduction in gastric mucosal DNA synthesis. These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

Conclusions: Treatment with obestatin increases gastric mucosal blood flow and cell proliferation, leading to acceleration of healing of gastric ulcers. These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

Show MeSH

Related in: MedlinePlus

Effect of saline (NaCl), induction of gastric ulcers (GU) or administration of obestatin (OB) at the dose of 8 nmol/kg/dose on gastric mucosal expression of mRNA for TNF-α and β-actin, and densitometric analysis of TNF-α/β-actin ratio. Mean ±SEM. N=10 in each group of animals. * P<0.05 compared to saline-treated rats without induction of ulcers (control); ** P<0.05 compared to saline-treated rats with ulcers.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3539620&req=5

f5-medscimonit-17-8-br196: Effect of saline (NaCl), induction of gastric ulcers (GU) or administration of obestatin (OB) at the dose of 8 nmol/kg/dose on gastric mucosal expression of mRNA for TNF-α and β-actin, and densitometric analysis of TNF-α/β-actin ratio. Mean ±SEM. N=10 in each group of animals. * P<0.05 compared to saline-treated rats without induction of ulcers (control); ** P<0.05 compared to saline-treated rats with ulcers.

Mentions: Administration of obestatin at the dose of 8 nmol/kg/dose was without effect on the ratio of mRNA for TNF-α to mRNA for β-actin in gastric mucosa in rats without induction of ulcers (Figure 5). Induction of ulcers increased expression of mRNA for TNF-α by 360%. Treatment with obestatin at the dose 8 nmol/kg/dose reduced the ulcer-evoked increase in expression of TNF-α mRNA by 61%, but this value was still higher than that observed in control rats with intact mucosa.


Administration of obestatin accelerates the healing of chronic gastric ulcers in rats.

Dembiński A, Warzecha Z, Ceranowicz P, Cieszkowski J, Dembiński M, Ptak-Belowska A, Kuwahara A, Kato I - Med. Sci. Monit. (2011)

Effect of saline (NaCl), induction of gastric ulcers (GU) or administration of obestatin (OB) at the dose of 8 nmol/kg/dose on gastric mucosal expression of mRNA for TNF-α and β-actin, and densitometric analysis of TNF-α/β-actin ratio. Mean ±SEM. N=10 in each group of animals. * P<0.05 compared to saline-treated rats without induction of ulcers (control); ** P<0.05 compared to saline-treated rats with ulcers.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539620&req=5

f5-medscimonit-17-8-br196: Effect of saline (NaCl), induction of gastric ulcers (GU) or administration of obestatin (OB) at the dose of 8 nmol/kg/dose on gastric mucosal expression of mRNA for TNF-α and β-actin, and densitometric analysis of TNF-α/β-actin ratio. Mean ±SEM. N=10 in each group of animals. * P<0.05 compared to saline-treated rats without induction of ulcers (control); ** P<0.05 compared to saline-treated rats with ulcers.
Mentions: Administration of obestatin at the dose of 8 nmol/kg/dose was without effect on the ratio of mRNA for TNF-α to mRNA for β-actin in gastric mucosa in rats without induction of ulcers (Figure 5). Induction of ulcers increased expression of mRNA for TNF-α by 360%. Treatment with obestatin at the dose 8 nmol/kg/dose reduced the ulcer-evoked increase in expression of TNF-α mRNA by 61%, but this value was still higher than that observed in control rats with intact mucosa.

Bottom Line: Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis.These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Jagiellonian University Medical College, Cracow, Poland. mpdembin@cyf-kr.edu.pl

ABSTRACT

Background: Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis. The aim of the present study was to investigate the influence of obestatin administration on the healing of chronic gastric ulcers.

Material/methods: Chronic gastric ulcers were induced in rats by 100% acetic acid applied to the serosal surface of the gastric wall. Obestatin was given twice a day intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose for 6 days. Six days after induction of ulcers, rats were anesthetized and the stomach was exposed for measurement of gastric blood flow and ulcer area. Biopsy samples from the gastric mucosa were taken for determination of mucosal DNA synthesis and for measurement of gastric expression of mRNA for interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).

Results: Induction of gastric ulcers alone increased mucosal blood flow and tissue expression of mRNA for TNF-alpha and IL-1beta, whereas gastric mucosal DNA synthesis was reduced. In rats with gastric ulcers, administration of obestatin increased gastric mucosal blood flow, accelerated the healing rate of these ulcers and partly reversed the gastric ulcer-induced reduction in gastric mucosal DNA synthesis. These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

Conclusions: Treatment with obestatin increases gastric mucosal blood flow and cell proliferation, leading to acceleration of healing of gastric ulcers. These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.

Show MeSH
Related in: MedlinePlus