The Novel Anti-Ulcer Agent Ecabet Sodium (TA-2711) Eradicates Helicobacter pylori Colonizing on the Gastric Mucosa of Japanese Monkeys

Fukuda, Yoshihiro; Mizuta, T.; Yamamoto, I; Tamura, Kouichi; Shimoyama, Takashi

doi:10.3109/00365529409094885

Cited by 10 publications

(9 citation statements)

References 2 publications

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“…Ecabet, a locally acting antiulcer agent, is known to have anti-H. pylori activity, eradicating H. pylori colonization on the gastric mucosa of Japanese monkeys [25], and inhibiting the urease activity of H. pylori [36]. These results suggest that ecabet may have an anti-H. pylori effect.…”

Section: Discussionmentioning

confidence: 88%

“…Ecabet sodium (ecabet, C 20 H 26 Na 2 O 5 S 8 H 2 O) is known to inhibit peptic activity of gastric secretion [22] and to enhance the defensive activity of gastric mucosa [23], suggesting anti-inflammatory activity. In addition, ecabet has been shown to promote the eradication of H. pylori [24], and to alleviate H. pylori -induced gastric inflammation [22,23,25]. Furthermore, ecabet was found to suppress IL-8 secretion of neutrophils stimulated with H. pylori extracts [26], suggesting that ecabet may influence the upstream pathway of IL-8 gene expression in gastric epithelial cells infected with H. pylori .…”

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confidence: 99%

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Inhibition of Helicobacter pylori‐induced Nuclear Factor‐kappa B Activation and Interleukin‐8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells

Kim

Jung

et al. 2003

Helicobacter

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Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

Inhibition of Helicobacter pylori‐induced Nuclear Factor‐kappa B Activation and Interleukin‐8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells

Kim

Jung

et al. 2003

Helicobacter

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“…However, Ecabet sodium is an old antiulcer agent with demonstrated activity against H. pylori growth related to urease inhibition and reduction of the adhesion of bacteria on gastric mucosa [138][139][140][141]. It has been succesfully tested in H. pylori eradication, firstly in monkeys [142]. Then it has been studied in association with lansoprazole and amoxicillin or nitroimidazole: results have shown an increased eradication rate when compared to a dual therapy [143][144][145][146].…”

Section: Other Strategiesmentioning

confidence: 97%

Treatment of H. pylori Infection: A Review

Candelli

Nista²,

Carloni³

et al. 2005

CMC

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Helicobacter pylori infection has been indicated as the main pathogenic factor in the development of chronic gastritis, peptic ulcer disease, and gastric malignancies. Although the vast majority of infected subjects do not carry but a mild, asymptomatic gastritis, still there are some cases in which the eradication of the infection appears mandatory. This review addresses current anti-Helicobacter regimens and pharmacological resources, and highlights the pros and cons of each of them, according to the most recent and reliable clinical trials. Also, basic recommendations are given, regarding treatment choice in the event of the failure of a first or second line eradicating strategy, and about the implementation of standard regimens with newer antibacterial devices as probiotics.

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“…Ecabet has an eradicative effect on Helicobacter pylori. 13) Baričević et al 14) reported that the plasma cortisol levels of subjects infected with Helicobacter pylori were significantly higher than those of subjects not infected. It is not known how Helicobacter pylori infection is related to the HPA axis, and whether the anti-urease effect might be related to a modulatory effect on the HPA axis, however the modulatory effect is believed to be clinically useful.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Effects of Cytoprotective Drugs on Human Plasma Adrenocorticotropic Hormone and Cortisol Levels with Continual Stress Exposure

Katagiri

Shiga

Sato

et al. 2005

Biological & Pharmaceutical Bulletin

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The pathophysiology of acid-peptic disease may be thought of as an imbalance between aggressive factors (acid, pepsin and Helicobacter pylori infection) and local mucosal defenses; the secretion of bicarbonate, mucus and prostaglandins. Although treatment most often is directed at the reduction of aggressive factors, it can be directed at strengthening mucosal defenses of the stomach and the duodenum with so-called cytoprotective agents.Cetraxate hydrochloride (cetraxate), introduced in 1976 as an anti-ulcer drug with a mucosal protective effect, produces a dose-related increase in gastric mucosal blood flow, 1) and raises plasma calcitonin gene-related peptide and substance P levels, which are powerful vasoactive substances.2) Ecabet sodium (ecabet) and sulpiride have similar effects to cetraxate; an improvement of the gastric mucosal microcirculation and acceleration of bicarbonate secretion. 3,4) Gastric mucosal injury is greatly influenced by mental and/or physiological stress. The hypothalamo-pituitaryadrenal (HPA) axis is activated when stress is present. Corticotropin-releasing hormone (CRH) is secreted from the hypothalamus and stimulates the pituitary. From the pituitary, adrenocorticotropic hormone (ACTH), which stimulates adrenal and accelerates cortisol secretion, is secreted. ACTH and cortisol suppress the secretion of CRH (negative feedback) to normalize the HPA axis. Therefore, we believe that ACTH and cortisol may be indicators of stress.ACTH is a peptide containing 39 amino acids, and ACTHlike immunoreactive substance (IS) is found in tissues other than the pituitary gland (i.e., brain, adrenal gland, gastrointestinal tract, pancreas, thyroid gland, and placenta). The secretion of ACTH is controlled by a circadian rhythm mechanism and negative feedback from plasma cortisol and neurogenic stimulation.5) The peptide acts to secrete glucocorticoid and rises under stress. 6) Cortisol, commonly used to indicate the level of stress, is secreted by the zona fasciculate of the adrenal cortex and its secretion is dependent on the ACTH level.In general, venipuncture for blood sampling is thought to be a stress factor that can increase circulating ACTH and cortisol levels. 7) Repetitive blood sampling places subjects under artificial stress and venipuncture as a stressor is useful for the evaluation of the pharmacological effects of drugs. 8)To determine whether cytoprotective drugs can improve HPA axis abnormalities, which might be closely related to the genesis of peptic ulcers, we investigated the effects on stress-related hormone levels (ACTH-IS and cortisol) under continual stress after administration of cetraxate, ecabet and sulpiride. MATERIALS AND METHODSMaterials Cetraxate (Neuer capsule; Daiichi Seiyaku Co., Ltd., Tokyo, Japan), ecabet (Gastrom granules; Tanabe Seiyaku Co., Ltd., Osaka, Japan) and sulpiride (Dogmatyl capsule; Fujisawa Pharmaceuticals Co., Ltd., Osaka, Japan) were used. Lactose (Merck Hoei Co., Ltd., Osaka, Japan) was used as placebo.Synthetic human ACTH (1-10) was purchased from ...

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The Novel Anti-Ulcer Agent Ecabet Sodium (TA-2711) Eradicates Helicobacter pylori Colonizing on the Gastric Mucosa of Japanese Monkeys

Cited by 10 publications

References 2 publications

Inhibition of Helicobacter pylori‐induced Nuclear Factor‐kappa B Activation and Interleukin‐8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells

Inhibition of Helicobacter pylori‐induced Nuclear Factor‐kappa B Activation and Interleukin‐8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells

Treatment of H. pylori Infection: A Review

Comparison of the Effects of Cytoprotective Drugs on Human Plasma Adrenocorticotropic Hormone and Cortisol Levels with Continual Stress Exposure

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