Protective role of hydrogen-rich water on aspirin-induced gastric mucosal damage in rats

Zhang, Jingyao; Wu, Qifei; Wan, Yong; Song, Siyuan; Xu, Jia; Xu, Xiayu; Chang, He; Tai, Ming-Hui; Dong, Yafeng; Liu, Chang

doi:10.3748/wjg.v20.i6.1614

Cited by 37 publications

(24 citation statements)

References 45 publications

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“…Previous studies have documented that the mechanism of aspirin-induced gastric damage involves an inhibition of cytoprotective prostaglandin E 2 production via COX-1/ COX-2 enzymatic activity and the prominent fall in GBF leading to the formation of severe hemorrhagic lesions of gastric mucosa [5,[29][30][31][32][33]. On the other hand, recent studies reported that the endogenous gaseous mediators H 2 S, CO, and NO contribute to the maintenance of gastric mucosal integrity and prevent the formation of gastric mucosal lesions induced by various noxious stimuli, such as exposure to stress or administration of ethanol, bisphosphonates, and NSAIDs, including aspirin [5,17,19,21,22,26,34].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

et al. 2017

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Background Aspirin exerts side effects within the gastrointestinal tract. Hydrogen sulfide (H 2 S) and carbon monoxide (CO) have been implicated in gastroprotection but the mechanism of beneficial action of these gaseous mediators against aspirin-induced damage has not been fully studied. We determined the involvement of afferent sensory neurons, calcitonin-gene-related peptide (CGRP), lipid peroxidation, and nitric oxide (NO) biosynthesis in gastroprotection of H 2 S-releasing NaHS and CO-releasing tricarbonyldichlororuthenium(II) dimer (CORM-2) against aspirin-induced injury. Methods Wistar rats with or without capsaicin-induced denervation of sensory neurons were pretreated with vehicle, CORM-2 (5 mg/kg intragastrically), or NaHS (5 mg/kg intragastrically) with or without capsazepine (5 mg/kg intragastrically) or N G -nitro-L-arginine (L-NNA, 20 mg/kg intraperitoneally). The areas of aspirin-induced lesions and gastric blood flow (GBF) were assessed by planimetry and laser flowmetry respectively. Gastric mucosal messenger RNA and/or protein expression of CGRP, heme oxygenase 1, inducible nitric oxide synthase, cyclooxygenase 2, interleukin-1b, glutathione peroxidase 1 (GPx-1), and superoxide dismutase was determined by real-time PCR or Western blot. Malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) content was determined by colorimetric assay. Results Aspirin caused gastric lesions, decreased GBF, and raised MDA content, but pretreatment with NaHS and CORM-2 reduced these effects. Capsaicin-induced denervation or co-treatment with capsazepine reversed the gastroprotective and vasodilatory effects of NaHS but not those of CORM-2. L-NNA reversed NaHS-induced gastroprotection and partly reduced CORM-2-induced gastroprotection. NaHS and CORM-2 decreased MDA and 4-HNE content, restoring GPx-1 protein expression. Conclusions We conclude that H 2 S-but not CO-mediated gastroprotection against aspirin-induced injury involves afferent sensory nerves and partly NO activity. NaHS and CORM-2 prevented aspirin-induced gastric mucosal lipid peroxidation via restoration of microcirculation and antioxidative GPx-1 protein expression.

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Section: Discussionmentioning

confidence: 99%

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

et al. 2017

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“…8 For example, the pretreatment with hydrogen-rich water mitigated aspirin-induced gastric lesions via lessening oxidative stress and inflammatory reactions. 9 Hydrogen-rich saline suppressed the production of several proinflammatory mediators through inhibiting the activation of p38 and NF-jB. 10 Drinking hydrogen-rich water had anti-oxidative effect on aging periodontal tissues.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats

Liu

Geng

Jiang

et al. 2017

Exp Biol Med (Maywood)

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This study was designed to evaluate protective effect of hydrogen-rich saline, a novel antioxidant, on tobacco smoke (TS)-induced chronic obstructive pulmonary disease (COPD) in rats and explore the underlying mechanism. Our results suggest that administration of hydrogen-rich saline improves lung function and alleviates morphological impairments of lung through alleviating inflammation, reducing oxidative stress and lessening mucus hypersecretion in TS-induced COPD rats. AbstractChronic obstructive pulmonary disease induced by tobacco smoke has been regarded as a great health problem worldwide. The purpose of this study is to evaluate the protective effect of hydrogen-rich saline, a novel antioxidant, on chronic obstructive pulmonary disease and explore the underlying mechanism. Sprague-Dawley rats were made chronic obstructive pulmonary disease models via tobacco smoke exposure for 12 weeks and the rats were treated with 10 ml/kg hydrogen-rich saline intraperitoneally during the last 4 weeks. Lung function testing indicated hydrogen-rich saline decreased lung airway resistance and increased lung compliance and the ratio of forced expiratory volume in 0.1 s/forced vital capacity in chronic obstructive pulmonary disease rats. Histological analysis revealed that hydrogen-rich saline alleviated morphological impairments of lung in tobacco smoke-induced chronic obstructive pulmonary disease rats. ELISA assay showed hydrogen-rich saline lowered the levels of pro-inflammatory cytokines (IL-8 and IL-6) and anti-inflammatory cytokine IL-10 in bronchoalveolar lavage fluid and serum of chronic obstructive pulmonary disease rats. The content of malondialdehyde in lung tissue and serum was also determined and the data indicated hydrogen-rich saline suppressed oxidative stress reaction. The protein expressions of mucin MUC5C and aquaporin 5 involved in mucus hypersecretion were analyzed by Western blot and ELISA and the data revealed that hydrogen-rich saline down-regulated MUC5AC level in bronchoalveolar lavage fluid and lung tissue and up-regulated aquaporin 5 level in lung tissue of chronic obstructive pulmonary disease rats. In conclusion, these results suggest that administration of hydrogen-rich saline exhibits significant protective effect on chronic obstructive pulmonary disease through alleviating inflammation, reducing oxidative stress and lessening mucus hypersecretion in tobacco smoke-induced chronic obstructive pulmonary disease rats.

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“…The preliminary study was performed based on several previous studies, which mentioned that the dosage for ulcer induction is 200-400mg/kgBW. 6,14,15 Termination time for aspirin treatment in the previous research was done on the first and third days after treatment. 6,15 Preliminary study on aspirin induction Two aspirin dosages were used in the preliminary study, 200mg/kgBW and 400mg/kgBW.…”

Section: Resultsmentioning

confidence: 99%

“…6,14,15 Termination time for aspirin treatment in the previous research was done on the first and third days after treatment. 6,15 Preliminary study on aspirin induction Two aspirin dosages were used in the preliminary study, 200mg/kgBW and 400mg/kgBW. The termination time for 200mg/kgBW were days 3, 4, and 5 after treatment; and for 400mg/kgBW were days 1, 2, and 3 after treatment.…”

Section: Resultsmentioning

confidence: 99%

“…It has been explained in the previous study that the use of aspirin at lower dosage (75-300 mg) will gradually activate various disturbances of the digestion channel, such as dyspepsia, erosion of gastric wall, and ulcer with bleeding leading to perforation. 15 Moreover, another study stated that lesions of gastric mucosa caused by NSAID including aspirin will attain the peak on the third day after induction and decrease in the 10 th day. 17 Gastric ulcers are caused by local inflammation, which is initiated by the imbalanced production of mucus, bicarbonate and gastric acid resulting in gastric mucosa irritation.…”

Section: Discussionmentioning

confidence: 99%

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The expression of COX-2 and iNOS in ethanol and aspirin induced gastric ulcer rat models

2018

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Aspirin or ethanol induced gastric ulcer rat models are the most frequently used in studies. Aspirin and ethanol induced gastric ulcers through different pathways involving COX-2 and iNOS. The aim of this study was to examine the expression of COX-2 and iNOS in gastric ulcer rat model induced by ethanol and aspirin. Twenty-one Sprague Dawley rats were divided into 7 groups i.e. control group (CA), ethanol 1 st day (ED 1), ethanol 3 rd day (ED 3), ethanol 5 th day (ED 5), aspirin 4 th day (AD 4), aspirin 6 th day (AD 6), and aspirin 8 th day (AD 8). Oral administration of aspirin was at 200mg/kgBW and the 100% ethanol at 1mL/200gBW. Macroscopic and microscopic observations were done to examine the gastric mucosal damage, COX-2 and iNOS expressions. Severe gastric ulcers were observed in ED 1 and AD 4 groups and mild gastric mucosal damage was observed in ED 3 , ED 5 , AD 6 and AD 8 groups. Microscopically, light erosion was shown by the CA and AD 8 groups. Erosion was also shown by ED 3 , ED 5 , and AD 6 groups. The most severe damage with ulcers and heavier bleeding were shown by the ED 1 and AD 4 groups. Weak COX-2 expression was found in the CA, while the highest COX-2 expression was found in the ED 1. The iNOS expression in the ethanol groups was still increasing until the 5 th day (ED 5). In the aspirin groups, it reached the peak on the 3 rd day (AD 6), and already declined on the 5 th day (AD 8). In conclusion, the damage process of ethanol induced gastric ulcer occurred faster than that by aspirin. The highest COX-2 expression in the ethanol and aspirin groups were shown at the onset begin. iNOS expression in ethanol induced ulcer groups still increased until the 5 th day, while in the aspirin induced ulcer groups already declined in the 5 th day. ABSTRAK Tikus model ulkus lambung yang diinduksi oleh aspirin atau etanol adalah model yang paling sering digunakan dalam penelitian. Ulkus lambung yang diinduksi aspirin mempunyai jalur pathogenesis yang berbeda dengan yang diinduksi oleh etanol, namun keduanya melibatkan COX-2 dan iNOS. Tujuan penelitian ini adalah mengkaji ekspresi COX-2 dan iNOS pada tikus model ulkus lambung yang diinduksi oleh ethanol dan aspirin. Dua puluh satu tikus Sprague Dawley dibagi menjadi 7 yaitu kelompok kontrol (CA), etanol hari pertama (ED 1), etanol hari ketiga (ED 3), etanol hari kelima (ED 5), aspirin hari keempat (AD 4), aspirin hari keenam (AD 6), dan aspirin hari kedelapan (AD 8). Perlakuan diberikan secara oral, dengan dosis aspirin sebesar 200 mg/kgBB dan dosis 100% etanol sebesar 1mL/200gBB. Pengamatan makroskopis dan mikroskopis dilakukan untuk menilai kerusakan mukosa lambung, ekspresi COX-2 dan iNOS. Ulkus lambung berat terlihat pada kelompok ED 1 dan AD 4 dan kerusakan mukosa lambung ringan terlihat pada kelompok ED 3 , ED 5 , AD 6 and AD 8. Secara mikroskopis, erosi ringan terlihat pada kelompok CA dan AD 8. Erosi juga terlihat kelompok ED 3 , ED 5 , dan AD 6. Kerusakan paling berat dengan ulkus dan pendarahan terlihat pada kelompok ED 1 dan AD 4. Ekspresi COX-2 le...

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Protective role of hydrogen-rich water on aspirin-induced gastric mucosal damage in rats

Cited by 37 publications

References 45 publications

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage

Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats

The expression of COX-2 and iNOS in ethanol and aspirin induced gastric ulcer rat models

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