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Ga, Cook; Sl, Elliott; Mv, Skeljo; As, Giraud; Yeomans, Neville D

doi:10.1023/a:1018828016573

Cited by 7 publications

(1 citation statement)

References 6 publications

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“…If the injury is restricted to the surface epithelium and the basal lamina is preserved, the denuded surface would be rapidly covered by migration of intact viable cells, restoring the mucosal integrity within hours [1, 2, 3]. This process of the epithelial restitution, the rate of which would be critical to the ultimate generation of gastric damage, has been shown to be influenced by various biological factors such as prostaglandins (PGs), nitric oxide (NO) and growth factors, through maintaining the microclimate around the injury [4, 5, 6, 7]. …”

Section: Introductionmentioning

confidence: 99%

Effect of Ecabet Disodium, a Novel Locally-Acting Antiulcer Drug, on Epithelial Restitution following Injury by Hypertonic NaCl in Bullfrog Stomach in vitro

Furukawa¹,

Kume²,

Sugamoto³

et al. 2000

Digestion

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Background: The antiulcer drug ecabet 2Na (12-sulfodehydroabietic acid disodium salt) exhibits a gastroprotective activity, mainly through a local action, involving endogenous prostaglandins (PGs) and nitric oxide (NO). In the present study, we examined the effect of ecabet on the epithelial restitution of the bullfrog gastric mucosa in vitro following injury by hypertonic NaCl. Methods: Bullfrog fundic mucosa was mounted in an Ussing chamber. The tissue injury was induced by exposure of the mucosa to 1.25 M NaCl for 5 min, and transmucosal potential difference (PD) and electrical resistance (R) were measured during a 4-hour test period. Ecabet (3–30 mg/ml) was added to the luminal solution for 10 min before or after NaCl, while 16,16-dimethyl PGE₂ (dmPGE₂: 1× 10^–6 M) or NOR-3 (a NO donor: 1 × 10^–4 M) was added to the nutrient solution 10 min before NaCl. Results: Mucosal application of 1.25 M NaCl caused an immediate reduction of PD and R, followed by a gradual normalization, reaching about 70% of the pre-exposure levels within 4 h. Ecabet, added before NaCl, significantly expedited the recovery of PD and R in a concentration-dependent manner; this effect was mimicked by posttreatment with ecabet and significantly mitigated by prior addition of indomethacin (1 × 10^–5 M) or N^G-nitro-L-arginine methyl ester (L-NAME: 1 × 10^–3 M). The epithelial restitution was also significantly promoted by serosal application of either dmPGE₂ or NOR-3. The mucosal exposure to ecabet significantly increased the luminal release of PGE₂ and NO metabolites, the effects being attenuated by indomethacin and L-NAME, respectively. The mucous secretion was increased by ecabet as well as dmPGE₂ and NOR-3, and the effect of ecabet was significantly suppressed by both indomethacin and L-NAME. The inhibitory effects of L-NAME on the ecabet action were all significantly antagonized by concurrent addition of L-arginine. Conclusion: These results suggest that ecabet significantly expedited the restitution following gastric surface cell injury, and this action is mediated by endogenous NO as well as PGs and may be functionally associated with an increase of mucous secretion.

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Section: Introductionmentioning

confidence: 99%

Effect of Ecabet Disodium, a Novel Locally-Acting Antiulcer Drug, on Epithelial Restitution following Injury by Hypertonic NaCl in Bullfrog Stomach in vitro

Furukawa¹,

Kume²,

Sugamoto³

et al. 2000

Digestion

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Involvement of Cyclooxygenase-2–Prostaglandin E2 Pathway in Interleukin-8 Production in Gastric Cancer Cells

et al. 2006

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Prostaglandin E(2) (PGE(2)) is thought to play an important role in both inflammatory and anti-inflammatory effects. The effect of PGE(2) on the proinflammatory chemokine interleukin-8 (IL-8) in the gastric epithelial cells has not been defined yet. A gastric cancer cell line (MKN45) and primary gastric fibroblasts were cocultured with Helicobacter pylori standard strain (NCTC11637). The expressions of IL-8 and cyclooxygenase 2 (COX-2) mRNA were examined by reverse transcription polymerase chain reaction (RT-PCR) amplification. The amount of IL-8 antigen secreted by the MKN45 cells and gastric fibroblasts was measured by enzyme-linked immunosorbent assay (ELISA). We examined the effects of H pylori stimulation on IL-8 and COX-2 expression levels and the effects of COX-2 inhibitor on H pylori-induced IL-8 production in the MKN45 cells and gastric fibroblasts. Furthermore, we examined the expressions of subtypes of PGE(2) receptors, the effects of arachidonic acid and PGE(2) on IL-8 production, and the effects of PGE(2) on the total cellular cyclic adenosine monophosphate (cAMP) in MKN45 cells. MKN45 cells and gastric fibroblasts expressed IL-8 and COX-2 mRNA under stimulation with H pylori. The MKN45 cells produced IL-8 and PGE(2) antigen into the culture medium with H pylori stimulation, and the production level of IL-8 and PGE(2) antigen decreased significantly with COX-2 inhibitor pretreatment (concentration: 50 muM). On the other hand, the gastric fibroblasts strongly produced IL-8 antigen even in the unstimulated condition, and the amount of IL-8 antigen was not affected by H pylori stimulation and/or COX-2 inhibitor pretreatment. The MKN45 cells expressed IL-8 mRNA and released IL-8 antigen slightly, and the expression level of IL-8 mRNA and the amount of IL-8 antigen increased significantly with PGE(2) treatment in a dose-dependent manner. PGE(2)-induced IL-8 production was inhibited by pretreatment with EP2 and EP4 antagonists. The MKN45 cells expressed EP2 and EP4 subtypes of PGE(2) receptors, and these expression levels were not affected by H pylori stimulation or PGE(2) treatment. The amount of IL-8 antigen increased slightly, but not significantly, with arachidonic acid treatment. PGE(2) treatment for 15 minutes increased the total cellular cAMP in the MKN45 cells. These results suggest that the COX-2-PGE(2) pathway may be involved in IL-8 production in gastric epithelial cells.

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Physiopathologie des lésions gastro-duodénales induites par les anti-inflammatoires non stéroïdiens

Lamarque

2004

Gastroentérologie Clinique et Biologique

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Untitled

Cited by 7 publications

References 6 publications

Effect of Ecabet Disodium, a Novel Locally-Acting Antiulcer Drug, on Epithelial Restitution following Injury by Hypertonic NaCl in Bullfrog Stomach in vitro

Effect of Ecabet Disodium, a Novel Locally-Acting Antiulcer Drug, on Epithelial Restitution following Injury by Hypertonic NaCl in Bullfrog Stomach in vitro

Involvement of Cyclooxygenase-2–Prostaglandin E2 Pathway in Interleukin-8 Production in Gastric Cancer Cells

Physiopathologie des lésions gastro-duodénales induites par les anti-inflammatoires non stéroïdiens

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