Protective Effects of Simvastatin Against Alendronate-Induced Gastric Mucosal Injury in Rats

ABSTRACT Radon therapy using radon (222Rn) gas is classified into two types of treatment: inhalation of radon gas and drinking water containing radon. Although short- or long-term intake of spa water is effective in increasing gastric mucosal blood flow, and spa water therapy is useful for treating chronic gastritis and gastric ulcer, the underlying mechanisms for and precise effects of radon protection against mucosal injury are unclear. In the present study, we examined the protective effects of hot spring water drinking and radon inhalation on ethanol-induced gastric mucosal injury in mice. Mice inhaled radon at a concentration of 2000 Bq/m3 for 24 h or were provided with hot spring water for 2 weeks. The activity density of 222Rn ranged from 663 Bq/l (start point of supplying) to 100 Bq/l (end point of supplying). Mice were then orally administered ethanol at three concentrations. The ulcer index (UI), an indicator of mucosal injury, increased in response to the administration of ethanol; however, treatment with either radon inhalation or hot spring water inhibited the elevation in the UI due to ethanol. Although no significant differences in antioxidative enzymes were observed between the radon-treated groups and the non-treated control groups, lipid peroxide levels were significantly lower in the stomachs of mice pre-treated with radon or hot spring water. These results suggest that hot spring water drinking and radon inhalation inhibit ethanol-induced gastric mucosal injury.

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Protective effects of DIDS against ethanol-induced gastric mucosal injury in rats

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmp014 ◽

2009 ◽

Vol 41 (4) ◽

pp. 301-308 ◽

Cited By ~ 38

Author(s):

W. Zhao ◽

F. Zhu ◽

W. Shen ◽

A. Fu ◽

L. Zheng ◽

...

Keyword(s):

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Protective Effects

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The Gastroprotective Effect of Small Molecule Oligopeptides Isolated from Walnut (Juglans regia L.) against Ethanol-Induced Gastric Mucosal Injury in Rats

Nutrients ◽

10.3390/nu12041138 ◽

2020 ◽

Vol 12 (4) ◽

pp. 1138 ◽

Cited By ~ 2

Author(s):

Rui Liu ◽

Yun-Tao Hao ◽

Na Zhu ◽

Xin-Ran Liu ◽

Jia-Wei Kang ◽

...

Keyword(s):

Body Weight ◽

Gastric Content ◽

Juglans Regia ◽

Antioxidant Properties ◽

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Gastric Injury ◽

Protective Effects ◽

Sprague Dawley ◽

Gastroprotective Effect

The study investigated the protective effect of walnut oligopeptides (WOPs) against ethanol-induced gastric injury using Sprague-Dawley (SD) rats. Rats were randomly divided into seven groups based on body weight (10/group), normal group, ethanol group, whey protein group (220 mg/kg body weight), omeprazole group (20 mg/kg body weight), and three WOPs groups (220, 440, 880 mg/kg body weight). After 30 days of treatment with WOPs, rats were given 5 mL/kg absolute ethanol by gavage to induce gastric mucosal injury. Gastric ulcer index (GUI) were determined and the following measured; gastric content pH, gastric mucin, endogenous pepsinogens (PG), prostaglandin E2 (PGE2), inflammatory cytokines, oxidative stress indicators, and the expression of apoptosis-related proteins were measured to evaluate the gastroprotective effect of WOPs. The results showed that the administration with WOPs markedly mitigated the hemorrhagic gastric lesions caused by ethanol in rats, and decreased the GUI, the gastric content pH, PG1, PG2, and NO levels, enhanced mucin and PGE2. Also, WOPs repressed gastric inflammation through the reduction of TNF-α, IL-6, IL-1β and increase IL-10 levels, and revealed antioxidant properties with the enhancement of superoxide dismutase, glutathione, and catalase activity, while reduction of malondialdehyde. Moreover, WOPs treatment significantly down-regulated Bax, caspase-3 and nuclear factor-κB p65 (NF-κB p65) expression, while up-regulating the expression of Bcl-2 and inhibitor kappa Bα (IκBα) protein. These results indicated that WOPs have protective effects against ethanol-induced gastric mucosal injury in rats through anti-inflammatory, anti-oxidation, and anti-apoptosis mechanisms.

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Reduction of asymmetric dimethylarginine in the protective effects of rutaecarpine on gastric mucosal injury

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y08-073 ◽

2008 ◽

Vol 86 (10) ◽

pp. 675-681 ◽

Cited By ~ 17

Author(s):

Ying-Zi Liu ◽

Yuan Zhou ◽

Dai Li ◽

Li Wang ◽

Gao-Yun Hu ◽

...

Keyword(s):

Asymmetric Dimethylarginine ◽

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Protective Effects ◽

Adma Level ◽

Ulcer Index ◽

Calcitonin Gene ◽

Vitro Effect

Our recent study has shown that asymmetric dimethylarginine (ADMA) plays an important role in facilitating gastric mucosal injury by multiple factors. To explore whether the protection of rutaecarpine against gastric mucosal injury is related to reduction of ADMA content, a model of ethanol-induced gastric mucosal injury in rats was selected for this study. The ulcer index, the content of ADMA and NO, and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in gastric tissues were measured in vivo after pretreatment with rutaecarpine. The in vitro effect of rutaecarpine on the release of calcitonin gene-related peptide (CGRP) and NO from isolated gastric tissues was also determined. The results showed that ethanol significantly increased the ulcer index, decreased the DDAH activity and the NO level, and elevated the ADMA level, which was attenuated by pretreatment with rutaecarpine (0.6 mg/kg or 1.2 mg/kg). In the isolated gastric tissues, rutaecarpine significantly increased the release of both CGRP and NO; the release of NO, but not CGRP, was abolished in the presence of l-NAME (10−4 mol/L). The present results suggest that rutaecarpine protects the gastric mucosa against injury induced by ethanol and that the gastroprotection of rutaecarpine is related to reduction of ADMA levels through stimulating the release of CGRP.

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