Effects of geranygeranylacetone on gastrointestinal secretion in rats

Fujimoto, Masatoshi; Yamanaka, Takashi; Bessho, Motoaki; Igarashi, Toshiji

doi:10.1016/0014-2999(82)90004-8

Cited by 23 publications

(10 citation statements)

References 11 publications

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“…Its protective effect on the gastric mucosa has been shown in studies of gastric injury induced by cold-or water immersion-restraint stresses, and by NSAIDs [17][18][19][20][21][22]. In the present study, long-term teprenone treatment reduced neutrophil infiltration and H. pylori colonization of the corpus.…”

Section: Discussionsupporting

confidence: 65%

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

Miyake¹,

Tsukui

Shinji

et al. 2004

Helicobacter

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Section: Discussionsupporting

confidence: 65%

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

Miyake¹,

Tsukui

Shinji

et al. 2004

Helicobacter

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“…7. TNF-α was used as a positive control [1,[28][29][30]. It has been suggested that GGA stimulates the synthesis and secretion of mucin by cultured gastric mucussecreting cells without increasing their production of PGs.…”

Section: Discussionmentioning

confidence: 99%

Geranylgeranylacetone Induces Cyclooxygenase-2 Expression in Cultured Rat Gastric Epithelial Cells Through NF-κB

Nishida

Yabe

et al. 2007

Dig Dis Sci

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Geranylgeranylacetone (GGA) effectively protects the gastric mucosa against noxious agents. The precise mechanisms underlying the gastroprotective actions of GGA are not known. To elucidate the precise mechanism of GGA, the effect of GGA treatment on COX-2 expression in rat gastric epithelial (RGM1) cells was investigated. We used a prostaglandin E2 (PGE2) enzyme-linked immunoassay kit and Western blot analysis to measure PGE2 production and COX-2 induction by GGA treatment in serum-starved RGM1 cells. Gel-shift assay, Western blot analysis, and a reporter assay were performed to determine which COX-2 promoter was involved in GGA-induced COX-2 expression. GGA treatment dose dependently increased COX-2 expression and PGE2 production. The nuclear factor (NF)-kappaB sites of the COX-2 gene promoter were critical for GGA-mediated COX-2 expression. GGA induces COX-2 expression and increases PGE2 production in serum-starved RGM1 cells via activation of the NF-kappaB sites of COX-2 gene promoters.

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“…GGA is an acyclic polyisoprenoid and an antiulcer drug developed in Japan (22). GGA has been shown to effectively protect gastric mucosa against several types of insults by increasing the synthesis and secretion of gastric mucin (23) without affecting gastric acid secretion (24,25) or prostaglandin expression. We found that GGA protected against ethanol-induced gastric damage by increasing MUC5AC and MUC6 levels rather than MUC1.…”

mentioning

confidence: 99%

Gastric Mucosal Protection via Enhancement of MUC5AC and MUC6 by Geranylgeranylacetone

et al. 2005

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The mucus layer that covers gastric mucosa is a powerful barrier that protects tissues from the hazardous gastric environment; however, the role of each gastric MUC type, such as MUC1, MUC5AC, and MUC6, has not been evaluated. The purpose of this study is to identify the MUC type, which plays a predominant role in this protective process by use of geranylgeranylacetone (GGA), a promising cytoprotective agent. In addition, the mechanism of mucus secretion promoted by GGA was investigated. Rat gastric mucosal damage was provoked using ethanol, and GGA was pretreated 1 hour before ethanol. GGA was found to significantly protect rats from ethanol-induced gastric damage by increasing mucus levels, MUC5AC and MUC6, especially at ethanol-induced ulcer margins, but not by MUC1. When expression of heat shock protein 70 (HSP70) and neuronal nitric oxide synthase (nNOS) was evaluated by Western blotting, both were found to be increased in GGA-treated ethanol rats. In addition, the cytoprotective effect of GGA was blocked by L-NMMA, a nonspecific NOS inhibitor, but not blocked by aminoguanidine, a specific inducible nitric oxide synthase inhibitor, thus indicating the participation of nNOS. In conclusion, GGA protected ethanol-induced gastric damage by upregulating MUC5AC and MUC6 rather than MUC1. In addition, HSP70 and nNOS were found to be involved in GGA cytoprotection, probably by increasing mucus production or secretion.

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Effects of geranygeranylacetone on gastrointestinal secretion in rats

Cited by 23 publications

References 11 publications

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

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

Geranylgeranylacetone Induces Cyclooxygenase-2 Expression in Cultured Rat Gastric Epithelial Cells Through NF-κB

Gastric Mucosal Protection via Enhancement of MUC5AC and MUC6 by Geranylgeranylacetone

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