Cytoprotective action of cetraxate against HClethanol-induced gastric lesion in rats.

Kurebayashi, Youichi; Ikeda, Takuya; Osada, Yasuaki

doi:10.1254/jjp.46.17

Cited by 19 publications

(8 citation statements)

References 20 publications

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“…ranged from 16 to 100 mg/kg, depending on the irritant. On the whole, the protective effect of TA-2711 against these necrotizing agents was more potent than that of cetraxate and sucralfate, both of which are known to exhibit gastric mucosal protective activity (9,10). The mode of the protective property of TA 2711 against different necrotizing agents was similar to that of PGE2 reported by Robert et al (3).…”

Section: Protective Effect Against Gastric Mucosal Lesionssupporting

confidence: 72%

Effects of 12-sulfodehydroabietic acid monosodium salt (TA-2711), a new anti-ulcer agent, on gastric mucosal lesions induced by necrotizing agents and gastric mucosal defensive factors in rats.

Onoda¹,

Takido²,

Magaribuchi³

et al. 1990

Jpn.J.Pharmacol

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Abstract-Effectsof TA-2711 on gastric mucosal lesions induced by various necrotizing agents and several defensive factors of gastric mucosa were investigated in rats. Oral administration of TA-2711 at 12.5 to 200 mg/kg prevented the formation of gastric mucosal lesions induced by 99.5% ethanol, 0.6 N HCI, 0.2 N NaOH and boiling water with ED50 values of 24, 58, 16 and 101 mg/kg, respectively. Oral TA-2711 at 100 mg/kg increased the gastric mucosal prostaglandin E2 (PGE2) level without any change in transmucosal potential difference. A sustained decrease in gastric mucosal blood flow produced by intragastric administration of 99.5% ethanol was inhibited by oral TA-2711 (50, 100 mg/kg) and 16,16-dimethyl PGE2 (10 ucg/kg). The effect of TA-2711 on ethanol-induced decrease in blood flow was suppressed by indomethacin (10 mg/kg, s.c.). Oral TA-2711 (25-100 mg/kg) dose-dependently increased the amount of mucus adherent to the gastric mucosa.In addition, gastric HCO3 secretion was increased by intragastric TA 2711 at 2.5 and 5.0 mg/ml.These results suggest that TA-2711 enhances gastric mucosal resistance by increasing mucus and HCO3 secretion and by maintaining mucosal blood flow, and protects the gastric mucosa against various irritants. The effects of TA-271 1 appear to be mediated by mucosal prostaglandins such as PGE2.

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Section: Protective Effect Against Gastric Mucosal Lesionssupporting

confidence: 72%

Effects of 12-sulfodehydroabietic acid monosodium salt (TA-2711), a new anti-ulcer agent, on gastric mucosal lesions induced by necrotizing agents and gastric mucosal defensive factors in rats.

Onoda¹,

Takido²,

Magaribuchi³

et al. 1990

Jpn.J.Pharmacol

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“…25) HCl-ethanol instillation induces se- vere epithelial desquamation, deep mucosal necrosis and submucosal edema associated with leucocyte accumulation. 26) The suppression of prostaglandin synthesis by nonsteroidal anti-inflammatory drugs (NSAIDS), such as indomethacin, results in increased susceptibility to mucosal injury and gastroduodenal ulceration. Indomethacin inhibits both cyclooxygenase-1 (COX-1) and COX-2 as well as the production of prostaglandins in the stomach and intestines to maintain the mucous lining of the gastrointestinal tract.…”

Section: Discussionmentioning

confidence: 99%

Anti-ulcerogenic Effect and HPLC Analysis of the Caffeoylquinic Acid-Rich Extract from Ligularia stenocephala

Lee

Nugroho

Bachri

et al. 2010

Biological & Pharmaceutical Bulletin

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Peptic ulcers can be caused by food, stress, genetic, and environmental factors, 1) including Helicobacter pylori infection, abuse of steroidal-or non-steroidal anti-inflammatory drugs (NSAIDs), irregular eating habits, smoking, alcohol consumption, and psychological stress.2) Peptic ulcers result from defects in the mucosa and muscularis mucosa, as well as oxidative stress due to the increase of reactive oxygen species (ROS). 3) In Korea, the leaves of Ligularia stenocephala MATSUM. et KOIDZ. (Family Compositae) are consumed as an edible vegetable and used as a Chinese folk medicine for the treatment of edema and scrofula. 4) In eastern and western Asia, the genus Ligularia is used for the treatment of influenza, cough, ulcer, and tuberculosis. 5) Yoon et al. have reported that the leaf extract of L. stenocephala showed the highest antithrombotic activity among large numbers of edible and herbal plants.6) The root of L. stenocephala contain benzofuran derivatives (ligulachepalins, euparin, hydroxytremetone, 7) 5,6-dimethoxy-2-isopropenylbenzofuran, 8) and stenocephalain, 9) as well as two caffeoylquinic acid derivatives, 3,4-dicaffeoylquinic acid and 3,5-dicaffeoylquinic acid).6) However, caffeoylquinic acid levels of those plants have not been studied.Although L. stenocephala has been traditionally used to treat gastric cancer or gastric ulcers, these biological activities have not been scientifically verified. Therefore, we intended to find the preventive activity of the caffeoylquinic acid-rich fraction with potent peroxynitrite scavenging effect on the ulcers induced by HCl/ethanol-and indomethacin/ bethanechol-induced in mice. In addition, we attempted to find whether or not the wild vegetables such as Ligularia species containing high level of caffeoylquinic acids are beneficial for ulcer disease. The methanolic extract of L. stenocephala together with its BuOH-and Et 2 O soluble fractions were evaluated for their anti-ulcerogenic activity using mice, with the BuOH extract showing the best activity. The BuOH fraction contained 5-O-caffeoylquinic acid, 3,5-di-O-caffeoyl-muco-quinic acid, and 3,5-di-O-caffeoylquinic acid from HPLC analytical data.In Korea, three Ligularia species, Ligularia stenocephala, L. fischeri, and L. fischeri var. spiciformis, are used as edible vegetables. The three herbs are similar taxonomically and are called gondalbi, gomchwi and numchwi, respectively, in Korea. Distinguishing these species may be improved with HPLC chromatograms. Other Compositae family members also contain caffeoylquinic acids, including Aster species, 10) and Solidago species, 5,11) as well as L. stenocephala, 6) and L. fischeri var. spiciformis. 11)Caffeoylquinic acid chemically consists of the two parts of quinic acid moiety and phenylpropanoid moiety. The most common parent skeleton of those compounds is quinic acid while muco-quinic acid or epi-quinic acid are also uncommonly found. The most common phenylpropanoid is caffeic acid while the less common ones are p-coumaric acid and ferulic acid. Caffeoylqui...

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“…Instillation of HCl/ethanol into the stomach of rats induces severe epithelial desquamation, deep mucosal necrosis and submucosal edema associated with leucocyte accumulation. 30) The mucosal integrity of the stomach is maintained by multiple factors, including both paracrine and neuronal systems. Further work is required to elucidate the mechanism of the gastroprotective effects of R-etodolac as well as the anti-allodynic mechanism of S-etodolac.…”

Section: Discussionmentioning

confidence: 99%

The Enantiomers of Etodolac, a Racemic Anti-inflammatory Agent, Play Different Roles in Efficacy and Gastrointestinal Safety

Inoue

Nogawa

Ito

et al. 2011

Biological & Pharmaceutical Bulletin

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The therapeutic effects of non-steroidal anti-inflammatory drugs (NSAIDs) include anti-pyretic, analgesic and anti-inflammatory effects, while their adverse effects are primarily gastrointestinal (GI) and renal toxicity. The major therapeutic and adverse effects are mediated by the inhibition of cyclooxygenase (COX), which catalyzes the rate-limiting step in the formation of prostanoids from arachidonic acid. [1][2][3] There are two membrane-bound COX isoenzymes, the constitutively expressed COX-1 and the highly inducible COX-2. 4) COX inhibitors include conventional NSAIDs and COX-2-selective inhibitors. Conventional NSAIDs, at therapeutic doses, are non-selective COX inhibitors and inhibit both isoenzymes. The anti-inflammatory benefits of NSAIDs are primarily due to COX-2 inhibition, while inhibition of COX-1 often elicits GI toxicity. Etodolac is widely known as a COX-2-selective inhibitor. 5-7) It has good clinical anti-inflammatory efficacy and a good safety profile for the GI tract. 8) Many NSAIDs are chiral and are marketed as the racemate (which contains equal amounts of each enantiomer). The anti-inflammatory activity of NSAIDs and their inhibition of prostaglandin synthetase is largely stereospecific in favor of the S-enantiomer. 9) Etodolac too is a racemate consisting of S-and R-enantiomers, and S-etodolac inhibits prostaglandin synthesis in sheep vesicular glands and decreases hind-paw volume in established adjuvant arthritic rats. 10) Neuropathic pain is a common symptom caused by injury to peripheral or central nerves, and it can result from pathological changes induced by metabolic disease, viral infection, traumatic injury or chemotherapeutically induced nerve damage. Clinically, neuropathic pain is characterized by mechanical and thermal allodynia, hyperalgesia and spontaneous ongoing pain that are often refractory to treatment. 11) Patients with neuropathic pain do not respond to NSAIDs, and resistance or insensitivity to opiates is common. 12) We recently reported that etodolac attenuates allodynia in a mouse model of neuropathic pain. 13) The mechanism of the anti-allodynic effects of etodolac has not yet been established, but COX inhibition is unlikely to be involved because the COX inhibitors indomethacin and celecoxib do not attenuate the allodynia. There is still a question which enantiomer of etodolac produces the anti-allodynic effect in mice. And there is also a question whether the ulcerogenic activity of etodolac is attributable to the S-enantiomer alone.In the present study, we evaluated the inhibitory effects of the enantiomers of etodolac on COX-1 and COX-2. We also investigated the beneficial actions of racemic etodolac and its enantiomers, especially their anti-inflammatory effects, antiallodynic effects and ulcerogenic activity, in mouse and rat models. S-Etodolac, but not R-etodolac, inhibited COX-2 and showed anti-inflammatory and anti-allodynic effects, while R-etodolac showed a gastroprotective effect that may explain the low GI toxicity of racemic etodolac. MATERIALS AND...

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Cytoprotective action of cetraxate against HClethanol-induced gastric lesion in rats.

Abstract: Abstract-The protective effect

Cited by 19 publications

References 20 publications

Effects of 12-sulfodehydroabietic acid monosodium salt (TA-2711), a new anti-ulcer agent, on gastric mucosal lesions induced by necrotizing agents and gastric mucosal defensive factors in rats.

Effects of 12-sulfodehydroabietic acid monosodium salt (TA-2711), a new anti-ulcer agent, on gastric mucosal lesions induced by necrotizing agents and gastric mucosal defensive factors in rats.

Anti-ulcerogenic Effect and HPLC Analysis of the Caffeoylquinic Acid-Rich Extract from Ligularia stenocephala

The Enantiomers of Etodolac, a Racemic Anti-inflammatory Agent, Play Different Roles in Efficacy and Gastrointestinal Safety

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