Prevention of Gastric Ulcer Recurrence with Tetraprenylacetone

Nagasawa, Yasushige; Tatsuta, Masaharu; Ishiguro, Shigeo

doi:10.1080/00365529850166194

Cited by 9 publications

(4 citation statements)

References 11 publications

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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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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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“…GGA was originally developed as a mucosal protecting agent 20 years ago [24], and several mechanisms of its protection against noxious agents have been proposed. Earlier, it was reported [25] that GGA stimulates the mucus production by gastric mucosal cells, other studies [16, 17], however, have shown that the protective effect of GGA on the gastric mucosa is not abolished by NSAIDs which are known to inhibit the mucus production.…”

Section: Discussionmentioning

confidence: 99%

Geranylgeranylacetone Protects the Human Gastric Mucosa from Diclofenac-Induced Injury via Induction of Heat Shock Protein 70

et al. 2007

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Background/Aim: Geranylgeranylacetone (GGA) enhances gastric mucosal protection against nonsteroidal anti-inflammatory drugs by upregulating mucosal heat shock proteins (HSP), but the effects of GGA on the human gastric mucosa have not been well examined. This study was conducted to determine whether a clinical dose of GGA protects the human gastric mucosa from diclofenac (DIC)-induced gastric mucosal injury. Methods: The study group comprised 40 healthy volunteers: 20 subjects were randomly assigned to take either placebo (lactose 1.5 g/day) or GGA (150 mg/day) for 2 weeks (study 1), and 20 subjects were assigned to take DIC (75 mg/day) plus placebo (lactose 1.5 g/day) or DIC (75 mg/day) plus GGA (150 mg/day) for 2 weeks (study 2). In both studies, gastroscopic biopsy specimens were obtained before and after treatment. Mucosal HSP70 expression and DNA damage were analyzed by measuring the levels of HSP70 and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-OHdG), respectively. Results: In study 1, GGA increased the mucosal HSP70 expression without increasing the 8-OHdG production. In study 2, DIC treatment increased the 8-OHdG production, whereas the combination of GGA and DIC enhanced the HSP70 expression and attenuated the increase in 8-OHdG induced by DIC. Conclusion: The clinical dose of GGA enhanced the gastric mucosal HSP70 expression and inhibited the DIC-induced gastric mucosal damage in humans.

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“…Dental plaque has been implicated as a source of H. pylori by studies that used culture [1, 2, 26], biochemical tests [2, 26], nucleic acid analysis [20, 23, 27, 28, 29], and immunological assays [30, 31]. Several studies revealed a high prevalence of H. pylori in the oral cavity of people in developing countries, whereas in industrialized countries neither dental plaque nor dentures seemed to be an important reservoir for H. pylori .…”

Section: Discussionmentioning

confidence: 99%

<i>Helicobacter pylori</i> in the Oral Cavity Reflects Handling of Contaminants but Not Gastric Infection

Doré-Davin

Heitz

Yang³

et al. 1999

Digestion

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Helicobacter pylori colonises the gastric mucosa, but can also be found within the oral cavity. The presence of H. pylori was monitored in the oral cavity of 22 patients with duodenal ulcer, before and after antibiotic treatment and of 24 hospital employees who were or were not professionally exposed to H. pylori. Gastric infection was determined by breath test. Bacteria in the oral cavity were detected by nested PCR of samples containing saliva and dental plaque, using primers specific for 16S rRNA and ureC genes. Before treatment, 9 out of 22 infected ulcer patients harbored H. pylori in their oral cavity. Bacteria disappeared from the oral cavity of 3 of 7 cured patients. Twelve of 17 exposed subjects harbored H. pylori in their oral cavity, while no bacteria could be detected in the mouths of the 7 nonexposed subjects. Presence of bacteria in the oral cavity reflects handling of contaminants; it does not correlate with gastric infection and does not seem to promote it.

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Prevention of Gastric Ulcer Recurrence with Tetraprenylacetone

Abstract: Treatment with TAP plus omeprazole significantly decreases ulcer recurrence through TAP's improved mucosal restoration.

Cited by 9 publications

References 11 publications

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

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

Geranylgeranylacetone Protects the Human Gastric Mucosa from Diclofenac-Induced Injury via Induction of Heat Shock Protein 70

<i>Helicobacter pylori</i> in the Oral Cavity Reflects Handling of Contaminants but Not Gastric Infection

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