Nitric oxide donors increase mucus gel thickness in rat stomach

Brown, James F.; Hanson, Peter J.; Whittle, Brendan J.R.

doi:10.1016/0014-2999(92)90824-n

Cited by 152 publications

(134 citation statements)

References 2 publications

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“…Among these patterns, NO-mediated regulation is particularly important as it is associated with host defense and inflammatory responses (26) and also plays a pivotal role in gastric mucosal protection against damage induced by ethanol, stress, endotoxins and drugs (27). NOS activity is particularly high in gastric tissues (28), where NO helps maintain gastric tissue integrity (29), controls gastromucosal-derived blood flow (30) and increases gastric mucus synthesis and secretion (28). L-arginine, a NOS substrate, has been shown to facilitate gastric ulcer healing by increasing cell regeneration in stomach tissues (31).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Acer mono Max. sap on water immersion restraint stress-induced gastric ulceration

Park

Son

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. Acer mono Max. sap (AmMs) is called 'Gol-Li-Su' or 'Go-Lo-Soe' in Korean, which means 'water beneficial to the bones'. It is reported that the sap contains several types of minerals and sugars. In particular, the calcium concentration of the sap is 36.5 times higher than that of commercial mineral water. Apart from its anti-osteoporosis effect, no reports have addressed the biological activities of AmMs against degenerative diseases. In the present study, we investigated whether AmMs alleviates gastric ulcer-related symptoms in a stress-induced mouse model. To assess the effect of AmMs on gastric ulcer-like symptoms, we carried out a water immersion restraint (WIRE) test and found that AmMs has potential in alleviating gastric ulcers in a concentration-dependent manner. These results indicate that the nutritional factors of the sap mitigate the gastric ulcer-related symptoms caused by stress-induced gastric lesions in mice. AmMs-treated mice exhibited a significant decrease in the ulcer index as compared to those treated with omeprazole or L-arginine. To examine one potential mechanism underlying this effect, we performed reverse transcription-polymerase chain reaction to ascertain whether molecular markers were associated with the mitigation of the gastric lesions. Epithelial and/or tissue nitric oxide synthase (NOS) was assessed to determine whether or not the genes were down-regulated dose-dependently by the sap. The levels of these enzymes were found to be lower in the tissue samples treated with AmMs compared with the levels in the control samples. These findings collectively suggest that AmMs significantly protects the gastric mucosa against WIRE stress-induced gastric lesions, at least in part, by alleviating inducible NOS and/or neuronal NOS expression. IntroductionAcute gastric mucosal injury is a serious clinical problem worldwide. The symptoms cause severe gastric ulceritis and, with sustained exposure, eventually lead to gastric cancer. Researchers have developed many in vivo gastric lesion models: the water immersion restraint (WIRE) stress model, the indomethacin-induced model and the ethanol-induced model using animals (1). The WIRE model has previously been used to observe various aspects affecting the formation of and recovery from gastric mucosal lesions, including sulphydryls, prostaglandins, growth factors and polyamines (2). WIRE stress-induced gastric lesions have also been used to study the roles of cell death and gastric acid secretion in ulcerogenesis (3).In general terms, gastric lesions are a disorder of the gastric blockade, which typically protects against cavernous problems caused by hydrogen ions and other toxic substances generated in the lumen (4). One main component of the gastric barrier is gastric microcirculation; a disturbance in gastric mucosal perfusion results in the formation of lesions and ulcers, such as those that present in animal models of ischemic gastric lesions (5). Gastric blood flow is classically controlled by signaling molecules, such as prostagland...

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Section: Discussionmentioning

confidence: 99%

Protective effect of Acer mono Max. sap on water immersion restraint stress-induced gastric ulceration

Park

Son

et al. 2011

Experimental and Therapeutic Medicine

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“…Nonenzymatic NO production has been observed in the stomach (15) and mouth (14), on the surface of the skin (16), and in the ischemic heart (12). It has been suggested that intragastric NO generation in the acidic stomach is involved in killing various gut pathogens, and in the regulation of mucosal blood flow and mucus formation (35). On the other hand, the NO production in the oral cavity is reported to be less, due to a higher pH in the mouth than in the stomach (14).…”

Section: Figmentioning

confidence: 99%

Whole body detection and imaging of nitric oxide generation in mice following cardiopulmonary arrest: Detection of intrinsic nitrosoheme complexes

Kuppusamy

Shankar

Roubaud

et al. 2001

Magnetic Resonance in Med

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Ischemic tissues generate nitric oxide (NO) by direct reduction of tissue nitrite under the acidic conditions that occur during ischemia. In view of the important implications of this enzymeindependent mechanism of NO generation on the pathogenesis and treatment of tissue injury, the NO formation in mice subjected to cardiopulmonary arrest was measured and imaged. Real-time measurement of NO generation was performed by detection of naturally generated NO-heme complexes in tissues using L-band electron paramagnetic resonance (EPR) spectroscopy. To distinguish NO generated from nitrite, animals were labeled with isotopically enriched 15 N-nitrite. Mice were infused with nitrite (70 mg/kg, intravenous), cardiopulmonary arrest induced by an overdose of phenobarbital, and transferred to the EPR resonator. Measurements of NO generation were performed on the intact animal at the levels of the head, thorax, and abdomen. At the end of 3 hr, major organs were isolated and analyzed for their NO signal. The NO complexes were found to have maximum levels in lung, heart, and liver. Three-dimensional spatial mapping of the NO complex in the intact animal subjected to cardiopulmonary arrest was performed using EPR imaging techniques. The images also confirmed the maximum formation in the lungs, heart, and liver. The present data reveal that mice subjected to cardiopulmonary arrest generate large amounts of NO, which is nitrite mediated. The observed signal was largely due to heme-bound NO, which accounted for the high concentrations found in these organs. This increased NO formation during cardiopulmonary arrest could contribute to the difficulty of resuscitation after long periods of arrest. Magn Reson Med 45:700 -707, 2001.

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“…Of these mechanisms, NO-mediated regulation is particularly important, as it is involved in host defense and inflammatory responses (23), and also plays a critical role in gastric mucosal protection against injury induced by pressure, ethanol, stress and/or endotoxins (24). NOS activity is particularly high in gastric tissue (25), where NO helps maintain the integrity of the gastric epithelium (26), regulates gastric mucosal blood flow (27), and stimulates gastric mucus secretion and synthesis (25). The NO donor, glyceryl trinitrate, and the NOS substrate, L-arginine, have been shown to accelerate gastric ulcer healing in rats by increasing angiogenesis in the stomach (16).…”

Section: Discussionmentioning

confidence: 99%

Gastrodia elata Blume protects against stress-induced gastric mucosal lesions in mice

An¹,

Park²,

Heo³

et al. 2007

Int J Mol Med

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Abstract. Gastrodia elata Blume (GEB) is a traditional herbal plant that has been used in Asian countries for centuries as an anticonvulsant, analgesic, and also as a sedative for treating general paralysis, epilepsy, vertigo, and tetanus. Although numerous reports have addressed the effects of GEB against degenerative diseases, no previous study has examined the possible gastroprotective effects of GEB. Here, we examined the effects of pretreatment with GEB (0.02 ml/g, p.o.) in a mouse water immersion restraint (WIR) stressinduced gastric lesion model. Our results revealed that mice pretreated with GEB had significantly fewer gastric lesions than their respective controls. Moreover, GEB-treated mice showed significant decreases in serum and gastric nitric oxide (NO) levels to 50 and 28%, respectively. To examine one possible mechanism underlying this effect, we used reverse transcription-polymerase chain reaction (RT-PCR) to examine NOS mRNA expression in gastric lesion tissues. Our results revealed that the mRNA expression of inducible nitric oxide synthase (iNOS) was reduced by ~50% in GEB-pretreated mice versus the controls, whereas the mRNA expression levels of endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) remained unchanged. These findings collectively suggest that GEB significantly protects the gastric mucosa against WIR-induced gastric damage, at least in part by decreasing NO levels via suppression of iNOS mRNA expression.

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Nitric oxide donors increase mucus gel thickness in rat stomach

Cited by 152 publications

References 2 publications

Protective effect of Acer mono Max. sap on water immersion restraint stress-induced gastric ulceration

Protective effect of Acer mono Max. sap on water immersion restraint stress-induced gastric ulceration

Whole body detection and imaging of nitric oxide generation in mice following cardiopulmonary arrest: Detection of intrinsic nitrosoheme complexes

Gastrodia elata Blume protects against stress-induced gastric mucosal lesions in mice

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