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Published by on November 13, 2020

In vivo studies performed on the whole fruit or juice, peel, and flowers demonstrate antiulcer effect in a variety of animal models. Punica granatum L. (pomegranate, Family Lythraceae) is a deciduous tree distributed throughout the world. Acid reflux is the backward flow of stomach acid into the esophagus, aka the tube that connects the mouth to the stomach, says Peyton Berookim, MD, FACG, a Los Angeles-based double board-certified gastroenterologist and director of the Gastroenterology Institute of Southern California.Every time you swallow, he explains, a circular band of muscle around the bottom of your … The aim of the present paper is to summarize the evidence for or against the efficacy of PG for addressing inflammatory conditions of the gastro-intestinal tract. Gastric ischemia induced for 20 minutes by bleeding from the carotid artery produced a marked reduction of gastric mucosal blood flow (GMBF) up to 40–50% of basal values. In this study, COX-2 expression was not significantly modified by indomethacin treatment; conversely, EA significantly increased COX-1 and COX-2 expression in the ulcerated group [36]. Anti-inflammatory properties of PG and its major components have been widely described in the literature (for a review, see [12]). One potential consequence of host-microbial interactions is the development of mucosal inflammation, which can lead to gastritis and ulcer. Hydroalcoholic extract of PG (methanol : water 3 : 1) and its ellagic acid-rich fraction significantly attenuated the DSS-induced increase in the histamine level, suggesting a capacity to stabilize mast cells degranulation [53]. From all the studies taken into consideration in the present paper, some conclusions can be drawn. Both urolithins C and D as well as urolithin A demonstrated a high antioxidant activity in vitro (IC50 0.16, 0.33, and 13.6 μM, resp. Signs and symptoms of Crohn's disease in women. The mixture of metabolites reduced monocyte migration inhibiting IL-8 secretion induced by TNFα and ICAM-1 and VCAM-1 levels after stimulation with IL-1β [51]. On the contrary, acidity was significantly reduced by EA (5 mg/kg) treatment [38]. :). In the first study, the antiphlogistic effects of EA (50 μM) were evaluated in Caco-2 differentiated cells treated with a mixture of proinflammatory stimuli (IL-1β, TNF-α, IFN-γ, and LPS) on secretion and mRNA expression of different inflammatory biomarkers (IL-6, IL-8, MCP-1, and IL-10). In fact, it was demonstrated that only a very small percentage of polyphenols ingested with diet are absorbed in the small intestine, while the majority of them remain in the gut lumen, where they counteract and are metabolized by gut microbiota. well I am glad you will be feeling relief soon. The ulcerogenic effect of NSAIDs seems to be related to the inhibition of endogenous prostaglandin synthesis, although it has also been established that indomethacin modifies other protective mechanisms of the gastric mucosa, including gastric secretion and the permeability of the gastric mucosal barrier [34]. The extract, at the concentration of 50 μM (expressed as total phenols), significantly inhibited the secretion of the chemokine IL-8 and the production of NO upon stimulation by IL-1β or a mixture of proinflammatory stimuli. DSS administration in mice was also associated with an increase in histamine content in colonic tissue, indicating mast cell degranulation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as acetylsalicylic acid, indomethacin, and ibuprofen, are commonly used as analgesics in many acute and chronic inflammatory conditions. H. pylori, a Gram-negative bacterium that colonizes the stomach of humans and primates, is the most responsible pathogen for these inflammatory processes. PG ETs release EA in the gut, and this compound is poorly absorbed in the small intestine; conversely, EA is largely metabolized by human gut microflora in the intestinal lumen into urolithins, such as urolithins A and B, and urolithin-8-methyl ether [17, 18]. It has been proposed that the decrease of anthocyanin concentration after pancreatin bile salt digestion (as a simulation of small intestine digestion) could be partially explained by the transformation of the flavylium cation to the chalcone at the neutral pH [20]; however these hypotheses need to be confirmed by in vivo studies. These metabolites reach relevant plasma concentrations (3–5 μM) after PG juice consumption [19]. All these anti-inflammatory effects might be explained by the reduction of the expression of COX-2 and iNOS, through the inhibition of NF-κB-mediated transcriptional activation and preventing p38, JNK and ERK-1/2 MAPKs phosphorilation [55]; (ii) the second study analysed EA effect in a model of chronic colitis. Ive been in agony as its been getting really bad in the past few months. We will be providing unlimited waivers of publication charges for accepted research articles as well as case reports and case series related to COVID-19. The long permanence (up to 56 hrs in the colon before excretion [45]) of PG ellagitannins and the interaction with gut microbiota lead to the formation of many metabolites, that could explicate different biological activities at this level. No studies dealing with the effect of PG extracts on acetic acid-induced gastritis are present in the literature, whereas some studies on the pure compound EA occur. In another study, topical application of NH4OH (60 mM) produced a persistent reduction of gastric potential difference in the stomach made ischemic by bleeding and resulted in hemorragic damage 1 hr later. Pomegranate seed oil (PSO) is predominantly composed of triglycerides containing unsaturated fatty acids, as conjugated linolenic acids, oleic acid, linolenic acid, palmitic acid, and stearic acid. With the exception of EA, the effect of the pure compounds at the gastric level was not investigated; this should be carefully considered for the future studies, since these molecules appear to be unmodified at the gastric level. A couple of my friends were out in Dubai and one in Bahrain. [33]. Stress-Induced Gastritis. demonstrated that aqueous extract of PG peel (AEP) shows a gastroprotective effect in rats with ethanol-induced gastric lesions [32]. For example, cold pressed PG seed oil has been shown to possess anti-inflammatory activity since it inhibited in vitro both cyclooxygenase and lipoxygenase enzymes. Treatment with PuA prevented also TNF-α and bacterial fMLP-induced neutrophil degranulation, resulting in reduced MPO release and lower tissue injuries [63]. I tend to believe based on my symptoms and what I've read, however, that I had a low Vitamin B-12 level. report that EA significantly inhibited the occurrence of stress-induced gastric lesions at 5 mg/kg [38], whereas the effect of the other pure compounds, including ETs and ANs, was not investigated.

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