Gastrin, somatostatin, G and D cells of gastric ulcer in rats

Sun, Feng-Peng; Song, Yu-Gang; Cheng, Wei; Zhao, Tong; Yao, Yongli

doi:10.3748/wjg.v8.i2.375

Cited by 33 publications

(23 citation statements)

References 54 publications

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“…It was reported that the disordered ratio of G/D cells, which can secrete gastrointestinal hormones gastrin and somatostatin, could lead to gastrointestinal dysfunction in acetic acid induced gastric ulcer model [29] . Maybe BPC 157 can antagonize the agents induced damage by modulating the number of G and D cells and maintaining the stable circumstances of stomach.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

Xue¹,

Wu²,

Gao³

et al. 2004

WJG

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AIM:To investigate the protective effects of gastric pentadecapeptide BPC 157 on acute and chronic gastric ulcers in rats and to compare the results in therapy of human gastric ulcers by different administration methods. METHODS:Gastric pentadecapeptide BPC 157 was administered (initial single or continuous administration) into rats either intragastrically or intramuscularly before (induced acute gastric ulcer) or after (induced chronic gastric ulcer) the applications of inducing agents, and each animal was sacrificed to observe the protective effects of BPC 157 on gastric ulcers. RESULTS:Both intramuscular (im) and intragastric (ig) administration of BPC 157 could apparently reduce the ulcer area and accelerate the healing of induced ulcer in different models and the effect of im administered BPC 157 was better than that of ig. The rats treated with higher dosages (400 ng/kg, 800 ng/kg) of BPC 157 (im and ig) showed significantly less lesion (P<0.01 vs excipient or saline control), the inhibition ratio of ulcer formation varied between 45.7% and 65.6%, from all measurements except 400 ng/kg BPC 157 in pylorus ligation induced model (P<0.05), in which the inhibition rate was 54.2%. When im administered (800 ng/kg BPC 157) in three models, the inhibition ratio of ulcer formation was 65.5%, 65.6% and 59.9%, respectively, which was better than that of famotidine (its inhibition rate was 60.8%, 57.2% and 34.3%, respectively). Continuous application of BPC 157 (in chronic acetate induced gastric ulcer) could accelerate rebuilding of glandular epithelium and formation of granulation tissue (P<0.05 at 200 ng/kg and P<0.01 at 400 ng/kg and 800 ng/kg vs excipient or saline control). CONCLUSION:Both im and ig administered gastric pentadecapeptide BPC 157 can apparently ameliorate acute gastric ulcer in rats and antagonize the protracted effect of acetate challenge on chronic ulcer. The effect of im administration of BPC 157 is better than that of ig, and the effective dosage of the former is lower than that of the latter.

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Section: Discussionmentioning

confidence: 99%

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

Xue¹,

Wu²,

Gao³

et al. 2004

WJG

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“…Eeubi indicated that the persistent absence of somatostatin receptrors for several months after ulceration might be of pathophysiological significance for ulcer healing. Sun et al 126) examined plasma gastrin and somatostatin levels, as well as the number of G and D cells in the antrum and the G/D ratio, in rats with acetic acid ulcers. Sun found increased gastrin levels and G/D ratios, as well as decreased somatostatin levels after ulceration; nonetheless, such changes gradually returned to normal as healing progressed.…”

Section: Hormonesmentioning

confidence: 99%

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Okabe

Amagase

2005

Biological & Pharmaceutical Bulletin

207

166

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Four types of experimental chronic ulcer models, named acetic acid ulcer models, have been developed to examine the healing process of peptic ulcers, screen anti-ulcer drugs, and better evaluate the adverse effects of various anti-inflammatory drugs on the gastrointestinal mucosa. The model easily and reliably produces round, deep ulcers in the stomach and duodenum, allowing acetic acid ulcer production in mice, rats, Mongolian gerbils, guinea pigs, cats, dogs, miniature pigs, and monkeys. These ulcer models highly resemble human ulcers in terms of both pathological features and healing process. The models have been established over the past 35 years and are now used throughout the world by basic and clinical scientists. One of the characteristic features of acetic acid ulcers in rats is the spontaneous relapse of healed ulcers Ͼ100 d after ulceration, an endoscopically confirmed phenomenon. Indomethacin significantly delays the healing of acetic acid ulcers, probably by reducing endogenous prostaglandins and inhibiting angiogenesis in ulcerated tissue. Helicobacter pylori significantly delays healing of acetic acid ulcers and causes relapse of healed ulcers at a high incidence in Mongolian gerbils. Anti-secretory drugs (e.g. omeprazole), prostaglandin analogs, mucosal defense agents (e.g. sucralfate), and various growth factors all significantly enhance healing of acetic acid ulcers. Gene therapy with epidermal growth factor and vascular endothelial growth factor applied to the base of acetic acid ulcers in rats is effective in enhancing ulcer healing. Since an inhibitor of nitric oxide syntase prevents ulcer healing, nitric oxide might be involved in the mechanism underlying ulcer healing. We conclude that acetic acid ulcer models are quite useful for various studies related to peptic ulcers.

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“…Somatostatin, an important peptide for inhibiting cellular proliferation and differentiation, could slow down the growth of various kinds of cells by blocking the synthesis and/or secretion of many important cytokines and hormones [10][11][12][13][14] . On the other hand, extensive physiological effects of somatostatin and its analogues are mainly mediated by five subtypes of somatostatin receptors (SSTR), including SSTR 1 , SSTR 2 (SSTR 2a and SSTR 2b ), SSTR 3 , SSTR 4 and SSTR 5 .…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells

Pan¹,

Li²,

Lu³

et al. 2004

WJG

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AIM:To assess the effects of somatostatin on proliferation and apoptosis of activated rat hepatic stellate cells (HSCs). METHODS:HSCs isolated from the livers of adult SpragueDawley rats (weighing 400-500 g) by in situ perfusion and purified by single-step density gradient centrifugation with Nycodenz, became activated after 10 days' cultivation. Then the apoptotic rate of HSCs treated with different doses of somatostatin for 72 h, was assayed by acridine orange/ et hid ium br omi de flu ores cen t s tai nin g, ter min al deoxynucleotidyl transferase-mediated dUTP nick end labeling, transmission electron microscopy and flow cytometry, while the proliferation of HSCs was measured by MTT assay. Furthermore, the mechanisms of somatostatin were investigated by cytodynamic analysis. RESULTS:Somatostatin at the concentration of 10 -6

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Gastrin, somatostatin, G and D cells of gastric ulcer in rats

Abstract: In gastric ulcer, the increased gastrin secreted by G cells, the declined somatostatin secreted by D cells, and the disordered G/D cell ratio can lead to gastrointestinal dysfunction.

Cited by 33 publications

References 54 publications

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells

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Gastrin, somatostatin, G and D cells of gastric ulcer in rats

Abstract: In gastric ulcer, the increased gastrin secreted by G cells, the declined somatostatin secreted by D cells, and the disordered G/D cell ratio can lead to gastrointestinal dysfunction.

Cited by 33 publications

References 54 publications

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats

An Overview of Acetic Acid Ulcer Models<br>&mdash;The History and State of the Art of Peptic Ulcer Research&mdash;

Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells

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An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—