Teprenone, but not H2‐Receptor Blocker or Sucralfate, Suppresses Corpus <i>Helicobacter pylori</i> Colonization and Gastritis in Humans: Teprenone Inhibition of <i>H. pylori</i>‐Induced Interleukin‐8 in MKN28 Gastric Epithelial Cell Lines

Miyake, Kazumasa; Tsukui, Taku; Shinji, Yoko; Shinoki, Kei; Hiratsuka, Tetsuro; Nishigaki, Hitoshi; Futagami, Seiji; Wada, Ken; Gudis, Katya; Iwakiri, Katsuhiko; Yamada, Nobutaka; Sakamoto, Choitsu

doi:10.1111/j.1083-4389.2004.00209.x

Cited by 15 publications

(16 citation statements)

References 40 publications

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“…GGA has also been shown to reduce gastric mucosal myeloperoxidase activity, an indicator of neutrophil infiltration, during restraint stress in an animal experiment. We have also shown previously that 3-month administration of GGA in patients with H. pylori -infected gastritis decreases the activity index and colony density of H. pylori in the corpus of the stomach [18]. Thus, the observation that in this 2-week trial we saw no change in the activity index after GGA treatment indicates that long-term treatment, of at least 3 months duration, is necessary for a reduction in neutrophil infiltration in H. pylori -infected gastritis.…”

Section: Discussionmentioning

confidence: 59%

“…In the case of H 2 RA, there is a lack of histological improvement including neutrophil or mononuclear cell infiltration despite the curative effect of these drugs on gastric mucosal erosions, suggesting that the healing of gastric mucosal lesions is not accompanied by parallel histopathological changes in chronic gastritis [31]. In contrast, recent studies have shown that GGA can suppress gastritis in the human gastric mucosa [18]. An in vitro experiment in gastric mucosal epithelial cells has shown that GGA suppresses the production of interleukin-8, a key player in neutrophil infiltration.…”

Section: Discussionmentioning

confidence: 99%

“…GGA is now widely used to treat patients with gastric ulcers or chronic gastritis regardless of H. pylori infection, both in Japan and other Asian countries [15,16,17,18]. Moreover, it has also been shown to improve gastritis scores in H. pylori- infected patients.…”

Section: Introductionmentioning

confidence: 99%

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Comparison of the Effectiveness of Geranylgeranylacetone with Cimetidine in Gastritis Patients with Dyspeptic Symptoms and Gastric Lesions: A Randomized, Double-Blind Trial in Japan

et al. 2007

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Background and Aim: Controversy remains regarding the treatment of choice for chronic gastritis patients with dyspeptic symptoms when Helicobacter pylori eradication is not indicated or fails for their gastric lesions. A multicenter, randomized, double-blind trial was performed to compare the effectiveness of geranylgeranylacetone (GGA), a mucoprotective drug, against cimetidine (CIT), an H₂-receptor antagonist, on the treatment of erosions and petechial hemorrhage in H. pylori-infected patients with dyspeptic symptoms. Methods: 128 H. pylori-positive gastritis patients with mucosal erosions and/or petechial hemorrhage were randomized to receive 150 mg GGA t.i.d. or 400 mg CIT b.i.d. for 2 weeks. Improvement and cure rates on endoscopic findings, symptom disappearance rates, and changes in mucosal neutrophil infiltration were compared. Results: Endoscopic improvement rates were significantly higher in the GGA group (n = 50) than in the CIT group (n = 54; 86.0 vs. 64.8%, p = 0.014). Endoscopic cure rates were also significantly higher for GGA than for CIT (80.0 vs. 55.6%, p = 0.012). Symptom disappearance rates were 52.0% for GGA and 42.6% for CIT, but the difference was not significant. There was also no significant difference in mucosal neutrophil infiltration between the groups. Conclusion: GGA treatment appears to be more effective than CIT for chronic gastritis-associated erosion and petechial hemorrhage.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

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Comparison of the Effectiveness of Geranylgeranylacetone with Cimetidine in Gastritis Patients with Dyspeptic Symptoms and Gastric Lesions: A Randomized, Double-Blind Trial in Japan

et al. 2007

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“…One pharmacological inducer of Hsps is geranylgeranylacetone (GGA). GGA has been safely used in Japan in the clinical treatment of gastric ulcers (Shirakabe et al 1995;Nagasawa et al 1998;Miyake et al 2004;Qian et al 2007). GGA has been shown to induce Hsp70 in variety of tissues, including the gastric mucosa, heart, liver, brain, and cochlea (Hirakawa et al 1996;Ooie et al 2001;Oda et al 2002;Mikuriya et al 2005;Sone et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Taleb

Brandon

Lee

et al. 2009

Cell Stress and Chaperones

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Sensory hair cells of the inner ear are sensitive to death from aging, noise trauma, and ototoxic drugs. Ototoxic drugs include the aminoglycoside antibiotics and the antineoplastic agent cisplatin. Exposure to aminoglycosides results in hair cell death that is mediated by specific apoptotic proteins, including c-Jun N-terminal kinase (JNK) and caspases. Induction of heat shock proteins (Hsps) can inhibit JNK-and caspase-dependent apoptosis in a variety of systems. We have previously shown that heat shock results in robust upregulation of Hsps in the hair cells of the adult mouse utricle in vitro. In addition, heat shock results in significant inhibition of both cisplatin-and aminoglycoside-induced hair cell death. In this system, Hsp70 is the most strongly induced Hsp, which is upregulated over 250-fold at the level of mRNA 2 h after heat shock. Hsp70 overexpression inhibits aminoglycoside-induced hair cell death in vitro. In this study, we utilized Hsp70-overexpressing mice to determine whether Hsp70 is protective in vivo. Both Hsp70-overexpressing mice and their wildtype littermates were treated with systemic kanamycin (700 mg/kg body weight) twice daily for 14 days. While kanamycin treatment resulted in significant hearing loss and hair cell death in wild-type mice, Hsp70-overexpressing mice were significantly protected against aminoglycosideinduced hearing loss and hair cell death. These data indicate that Hsp70 is protective against aminoglycoside-induced ototoxicity in vivo.

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“…Pharmacological actions of GGA include stimulation of the synthesis of gastric mucus and induction of heat-shock proteins (HSPs) [10,11]. GGA induces HSP70 in rat small intestine and prevents ischemia reperfusion injury [12,13].…”

Section: Introductionmentioning

confidence: 99%

Geranylgeranylacetone Protects against Diclofenac-Induced Gastric and Small Intestinal Mucosal Injuries in Healthy Subjects: A Prospective Randomized Placebo-Controlled Double-Blind Cross-Over Study

Niwa

Nakamura²,

Miyahara³

et al. 2009

Digestion

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Background and Aims: Little information is available regarding the prevention and treatment of small intestinal mucosal injuries caused by non-steroidal anti-inflammatory drugs (NSAIDs). We planned a pilot study to investigate the protective effects of geranylgeranylacetone (GGA) against NSAID-induced small intestinal injuries using video capsule endoscopy (VCE). Subjects and Methods: Ten healthy male volunteers took oral GGA 300 mg/day (regimen A) or placebo (regimen B) in addition to diclofenac 75 mg/day + rabeprazole 20 mg/day for 7 days. We conducted a cross-over trial of regimens A and B with a 2-week washout period. All subjects underwent VCE before and after each administration period, and were evaluated for NSAID-induced gastric and small intestinal mucosal lesions. Results: The number of mucosal lesions (erosions, ulcers and a red spot with possible bleeding) detected in both stomach and small bowel changed between prior to and immediately after administration period, with significantly fewer lesions for regimen A after administration period (mean ± SD A:B = 2.6 ± 3.2:9.5 ± 8.5; p = 0.027). Conclusions: Combination therapy with GGA and rabeprazole reduced the incidence of gastroenteropathy induced by 1-week administration of diclofenac. Our findings suggest this therapy as a candidate for protecting patients on long-term NSAID therapy.

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Teprenone, but not H2‐Receptor Blocker or Sucralfate, Suppresses Corpus Helicobacter pylori Colonization and Gastritis in Humans: Teprenone Inhibition of H. pylori‐Induced Interleukin‐8 in MKN28 Gastric Epithelial Cell Lines

Abstract: Teprenone may modify corpus H. pylori-associated gastritis through its effect on neutrophil infiltration and H. pylori density, in part by its inhibition of IL-8 production in the gastric mucosa.

Cited by 15 publications

References 40 publications

Comparison of the Effectiveness of Geranylgeranylacetone with Cimetidine in Gastritis Patients with Dyspeptic Symptoms and Gastric Lesions: A Randomized, Double-Blind Trial in Japan

Comparison of the Effectiveness of Geranylgeranylacetone with Cimetidine in Gastritis Patients with Dyspeptic Symptoms and Gastric Lesions: A Randomized, Double-Blind Trial in Japan

Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Geranylgeranylacetone Protects against Diclofenac-Induced Gastric and Small Intestinal Mucosal Injuries in Healthy Subjects: A Prospective Randomized Placebo-Controlled Double-Blind Cross-Over Study

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