Role of Rebamipide on Induction of Heat-Shock Proteins and Protection Against Reactive Oxygen Metabolite-Mediated Cell Damage in Cultured Gastric Mucosal Cells

Hahm, Ki Baik; Park, In Suh; Kim, Young Soo; Kim, Jin Hong; Cho, Sung Won; Lee, Sang In; Youn, Jung Koo

doi:10.1016/s0891-5849(96)00406-6

Cited by 65 publications

(39 citation statements)

References 20 publications

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“…These results were inconsistent with those of Hong et al (1998), who noted similar effects of rebamipide against liver damage induced by endotoxic shock. Further, the present results confirmed previously reported data from several studies that comment on the anti-oxidant activity imparted by rebamipide (Hahm et al 1997;Kinjo et al 2008;Tokuhara et al 2008).…”

Section: Discussionsupporting

confidence: 92%

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Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂

Zakaria

El‐Sisi

2016

Journal of Immunotoxicology

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Prostaglandin E 2 (PGE 2 ) is a potent physiological suppressor of liver fibrosis. Because the anti-ulcer drug rebamipide can induce the formation of endogenous PGE 2 , this study investigated the potential effects of rebamipide on development of a hepatic fibrosis that was inducible by carbon tetrachloride (CCl 4 ). Groups of Wistar rats received intraperitoneal (IP) injections of CCl 4 (0.45 ml/kg [0.72 g CCl 4 /kg]) over the course of for 4 weeks. Sub-sets of CCl 4 -treated rats were also treated concurrently with rebamipide at 60 or 100 mg/kg. At 24 h after the final treatments, liver function and oxidative stress were indirectly assessed. The extent of hepatic fibrosis was evaluated using two fibrotic markers, hyaluronic acid (HA) and pro-collagen-III (Procol-III); isolated liver tissues underwent histology and were evaluated for interleukin (IL)-10 and PGE 2 content. The results indicated that treatment with rebamipide significantly inhibited CCl 4 -induced increases in serum ALT and AST and also reduced oxidative stress induced by CCl 4 . Fibrotic marker assays revealed that either dose of rebamipide decreased the host levels of Procol-III and HA that had become elevated due to the CCl 4 . At the higher dose tested, rebamipide appeared to be able to permit the hosts to have a normal liver histology and to minimize any CCl 4 -induced collagen precipitation in the liver. Lastly, the use of rebamipide was seen to be associated with significant increases in liver levels of both PGE 2 and the anti-inflammatory cytokine IL-10. Based on these findings, it is concluded that rebamipide can retard hepatic fibrosis induced by CCl 4 and that this effect may, in part, be mediated by an induction of PGE 2 and IL-10 in the liver itself. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 92%

“…The drug does this by aiding in the scavenging of hydroxyl radicals and other ROS (Hahm et al 1997(Hahm et al , 1998. In neutralizing ROS, many other antioxidants/drugs have been shown to induce anti-fibrotic effects (Cohen-Naftaly and Friedman 2011;Rosenbloom et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂

Zakaria

El‐Sisi

2016

Journal of Immunotoxicology

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“…; p < 0.05), and the protective effect of wogonin is superior to that of the well-known gastroprotectant, rebamipide (10,32). All these protections were achieved through early induction of PGD 2 synthesis and significant induction of apoptosis, based on other findings suggesting that the antiinflammatory action of PGD 2 is also very important in the prevention of dextran sodium sulfate-induced ulcerative colitis and the stress-induced gastritis model (17,18).…”

Section: Discussionmentioning

confidence: 94%

“…Although we investigated whether wogonin also influenced regenerating actions in damaged mucosa, no significant influences of wogonin pretreatment on the expression of vascular endothelial growth factor proteins (data not shown) were not observed except for a slight induction of HSP70 after 30 mg/kg wogonin treatment, similar to rebamipide (10,31,32). We also checked the changes in gastric mucin with immunohistochemical staining; there was no significant induction of any kind of mucin proteins after wogonin treatment despite small increases in expression, suggesting that the major action of wogonin against alcohol-induced gastropathy was antiinflammation.…”

Section: Discussionmentioning

confidence: 96%

Preventive Effect of the Flavonoid, Wogonin, Against Ethanol-Induced Gastric Mucosal Damage in Rats

Park

Hahm

et al. 2004

Dig Dis Sci

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Whether wogonin (5,7-dihydroxy-8-methoxyflavone), a flavonoid originated from the root of Scutellaria baicalensis Georgi, which has been shown to have antiinflammatory and antitumor activities in various cell types, possesses a gastric cytoprotective effect was investigated in an ethanol-induced gastric damage model in rats. Ethanol administration alone induced evident gastric damage including gastric hemorrhages and edema, while this gastric damage was significantly attenuated by wogonin pretreatment (30 mg/kg B.W.) 1 hr before ethanol administration. As major protective mechanisms of wogonin on ethanol-induced gastric damage, we found that wogonin showed either antiinflammatory effects through dual actions on arachidonic acid metabolism, i.e., induction of prostaglandin D 2 and suppression of 5S-hydroxyeicosatetraenoic acid (5S-HETE), or preventive induction of profuse apoptosis in the stomach. Conclusively, the flavonoid wogonin could be used as a preventive agent of alcohol-induced gastropathy, whose actions were proven to be strong antiinflammation and apoptosis induction.

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“…Therefore, by scavenging free radicals, the reactive oxygen metabolites might be useful by protecting the gastric mucosa from oxidative damage or by accelerating healing of gastric ulcers (5).…”

Section: Oxidative Stress In Gastric Mucosamentioning

confidence: 99%

Antioxidant properties of natural compounds used in popular medicine for gastric ulcers

Repetto

Llesuy

2002

Braz J Med Biol Res

432

277

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There is evidence concerning the participation of reactive oxygen species in the etiology and physiopathology of human diseases, such as neurodegenerative disorders, inflammation, viral infections, autoimmune pathologies, and digestive system disorders such as gastrointestinal inflammation and gastric ulcer. The role of these reactive oxygen species in several diseases and the potential antioxidant protective effect of natural compounds on affected tissues are topics of high current interest. To consider a natural compound or a drug as an antioxidant substance it is necessary to investigate its antioxidant properties in vitro and then to evaluate its antioxidant functions in biological systems. In this review article, we shall consider the role of natural antioxidants derived from popular plants to reduce or prevent the oxidative stress in gastric ulcer induced by ethanol.

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Role of Rebamipide on Induction of Heat-Shock Proteins and Protection Against Reactive Oxygen Metabolite-Mediated Cell Damage in Cultured Gastric Mucosal Cells

Cited by 65 publications

References 20 publications

Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂

Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂

Preventive Effect of the Flavonoid, Wogonin, Against Ethanol-Induced Gastric Mucosal Damage in Rats

Antioxidant properties of natural compounds used in popular medicine for gastric ulcers

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Role of Rebamipide on Induction of Heat-Shock Proteins and Protection Against Reactive Oxygen Metabolite-Mediated Cell Damage in Cultured Gastric Mucosal Cells

Cited by 65 publications

References 20 publications

Rebamipide retards CCl4-induced hepatic fibrosis in rats: Possible role for PGE2

Rebamipide retards CCl4-induced hepatic fibrosis in rats: Possible role for PGE2

Preventive Effect of the Flavonoid, Wogonin, Against Ethanol-Induced Gastric Mucosal Damage in Rats

Antioxidant properties of natural compounds used in popular medicine for gastric ulcers

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Product

Resources

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Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂

Rebamipide retards CCl₄-induced hepatic fibrosis in rats: Possible role for PGE₂