Gastroprotective actions of Taraxacum coreanum Nakai water extracts in ethanol-induced rat models of acute and chronic gastritis

Yang, Hye Jeong; Kim, Min Jung; Kwon, Dae Young; Kang, Eun Seon; Kang, Suna; Park, Sunmin

doi:10.1016/j.jep.2017.06.045

Cited by 37 publications

(21 citation statements)

References 35 publications

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“…Moreover, bioactive NO in the gastric lumen is regarded as a key defense factor that protects the gastric mucosa from noxious agents (26). Decrease of gastric blood flow is one cause of gastric mucosa injury induced by ethanol (27). However, NO can inhibit platelet aggregation and thrombosis, enhance the blood flow of gastric mucosa and cell regeneration, and improve mucosal repair (28).…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with Lactobacillus reuteri F-9-35 attenuates ethanol-induced gastric injury in rats

Sun¹,

Hou²,

Wang³

et al. 2018

Food & Nutrition Research

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BackgroundPrevious studies suggested that probiotics intervention may be one of the methods for preventing and/or treating gastric ulcer.ObjectiveThe aim of the study was to compare the preventive effects of a spaceflight mutant Lactobacillus reuteri F-9-35 and its wild type on ethanol-induced gastric injury in rats.DesignForty rats were randomly allocated into five groups: a normal group (NOR), ethanol group (EtOH), skim milk group (MILK), L. reuteri F-9-35 group (F935) and wild-type group (WT). The NOR and EtOH groups received 1 ml of distilled water by daily gavage for 14 days. The MILK group received 1 ml of skim milk alone, while the F935 and WT groups were administered 1 ml of skim milk containing the mutant and wild type (1 × 1010 colony-forming unit/ml) by daily gavage for 14 days, respectively. Acute gastric injury was induced by absolute alcohol 1 h after the final administration of different treatments, except for the NOR group.ResultsPretreatment with L. reuteri F-9-35, but not milk alone or milk with the L. reuteri wild type, showed significant reduction of ethanol-induced gastric injury, as evidenced by lowering of ulcer index, ulcer area (%), and histological lesion. F-9-35 decreased the levels of lipid peroxidation and myeloperoxidase and increased mucus, glutathione, and nitric oxide levels in gastric tissue. Moreover, F-9-35 inhibited the expression of proinflammatory genes including gastric tumor necrosis factor-α, interleukin-1β, and cyclooxygenase-2 and decreased the activity of nuclear factor kappa B (NF-κB).ConclusionThese findings indicated that L. reuteri F-9-35 pretreatment can attenuate ethanol-induced gastric injury in rats by inhibiting oxidative stress and inflammatory response. Together, L. reuteri F-9-35 has potential preventive efficacy on gastric ulcer.

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Section: Discussionmentioning

confidence: 99%

Pretreatment with Lactobacillus reuteri F-9-35 attenuates ethanol-induced gastric injury in rats

Sun¹,

Hou²,

Wang³

et al. 2018

Food & Nutrition Research

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“…Excessive alcohol consumption results in necrotic lesions in the gastric mucosa inducing acute hemorrhagic gastritis and ulcerative damage [ 4 , 5 ]. If untreated, gastritis progresses to gastric ulcer and carcinoma [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Liu

et al. 2020

Nutrients

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Alcohol consumption increases the risk of gastritis and gastric ulcer. Nutritional alternatives are considered for relieving the progression of gastric mucosal lesions instead of conventional drugs that produce side effects. This study was designed to evaluate the gastroprotective effects and investigate the defensive mechanisms of wheat peptides against ethanol-induced acute gastric mucosal injury in rats. Sixty male Sprague–Dawley rats were divided into six groups and orally treated with wheat peptides (0.1, 0.2, 0.4 g/kgbw) and omeprazole (20 mg/kgbw) for 4 weeks, following absolute ethanol administration for 1 h. Pretreatment with wheat peptides obviously enhanced the vasodilation of gastric mucosal blood vessels via improving the gastric mucosal blood flow and elevating the defensive factors nitric oxide (NO) and prostaglandin E2 (PGE2), and lowering the level of vasoconstrictor factor endothelin (ET)-1. Wheat peptides exhibited anti-inflammatory reaction through decreasing inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and increasing trefoil factor 1 (TFF1) levels. Moreover, wheat peptides significantly down-regulated the expression of phosphorylated nuclear factor kappa-B (p-NF-κB) p65 proteins in the NF-κB signaling pathway. Altogether, wheat peptides protect gastric mucosa from ethanol-induced lesions in rats via improving the gastric microcirculation and inhibiting inflammation mediated by the NF-κB signaling transduction pathway.

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“…Modern lifestyles and dietary habits, alcohol consumption, cigarette smoking, and stress are the less common causes of gastritis [2]. Inflammation and oxidative damage are commonly associated with gastric ulcer [3]. Oxidative damage is a serious problem in gastric ulcer [4].…”

Section: Introductionmentioning

confidence: 99%

Prodigiosins from a marine sponge-associated actinomycete attenuate HCl/ethanol-induced gastric lesion via antioxidant and anti-inflammatory mechanisms

et al. 2019

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Gastric ulcer is sores that form in the stomach mucosal layer because of erosion caused by high acid secretion and excessive use of non-steroidal anti-inflammatory drugs. Prodigiosins (PdGs) are red-pigmented secondary metabolites produced by bacteria, including actinomycetes. Butylcycloheptylprodigiosin ( 1 ) and undecylprodigiosin ( 2 ) were identified and isolated from a crude extract of the actinomycete RA2 isolated from the Red Sea Sponge Spheciospongia mastoidea . Chemical structure of 1 and 2 was determined by NMR and mass spectroscopy. Although their antioxidant and anti-inflammatory properties are known, their effect on gastric lesion is unknown. Therefore, this study aimed to investigate gastroprotective effects of PdGs against HCl/ethanol-induced gastric lesion in rats. Oral pretreatment with PdGs (100, 200, and 300 mg/kg) attenuated severity of HCl/ethanol-induced gastric mucosal injury, as evidenced by decreases in gastric lesion index scores, ulceration area, histopathologic abnormality, and neutrophil infiltration. These effects were comparable to those of omeprazole, a standard anti-gastric ulcer agent. HCl/ethanol-induced gastric erosions was associated with tremendous increases in lipid peroxidation, nitric oxide, and pro-inflammatory cytokines and mediators (myeloperoxidase, interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2), and with significant decreases in enzymatic and non-enzymatic antioxidant activities. However, PdGs ameliorated gastric inflammation and oxidative stress by downregulating nuclear factor kappa B and inducible nitric oxide synthase expression and upregulating heme oxygenase-1 expression. PdGs prevented gastric mucosal apoptosis by downregulating Bax and caspase-3 expression and upregulating Bcl-2 expression, thereby increasing prostaglandin E2 production. Our results suggested that PdGs exerted gastroprotective effects by decreasing the levels of inflammatory mediators, apoptotic markers, and antioxidants.

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Gastroprotective actions of Taraxacum coreanum Nakai water extracts in ethanol-induced rat models of acute and chronic gastritis

Cited by 37 publications

References 35 publications

Pretreatment with Lactobacillus reuteri F-9-35 attenuates ethanol-induced gastric injury in rats

Pretreatment with Lactobacillus reuteri F-9-35 attenuates ethanol-induced gastric injury in rats

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Prodigiosins from a marine sponge-associated actinomycete attenuate HCl/ethanol-induced gastric lesion via antioxidant and anti-inflammatory mechanisms

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