Fucoidan mitigates gastric ulcer injury through managing inflammation, oxidative stress, and NLRP3-mediated pyroptosis

Selim, Hend Mostafa; Negm, Walaa A.; Hawwal, Mohammed F.; Hussein, Ismail A.; Elekhnawy, Engy; Ulber, Roland; Zayed, Ahmed

doi:10.1016/j.intimp.2023.110335

Cited by 27 publications

(8 citation statements)

References 51 publications

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“…The presence of these active secondary metabolites in medicinal plants may contribute to a significant antiulcer and antioxidant effect. Oxidative stress, caused by an imbalance of free radicals and antioxidants, has been widely documented to cause and worsen peptic ulcers 69 . Additionally, oxygen-derived free radicals play a significant role in the pathogenesis of gastrointestinal mucosal damage 70 .…”

Section: Discussionmentioning

confidence: 99%

Ipomoea carnea mitigates ethanol-induced ulcers in irradiated rats via Nrf2/HO−1 pathway: an in vivo and in silico study

Ghareeb,

Mohammed,

Aboushousha

et al. 2024

Sci Rep

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The aim of this study was to investigate the potential of Ipomoea carnea flower methanolic extract (ICME) as a natural gastroprotective therapy against ethanol-induced gastric ulcers, particularly in individuals exposed to ionizing radiation (IR). The study focused on the Nrf2/HO−1 signaling pathway, which plays a crucial role in protecting the gastrointestinal mucosa from oxidative stress and inflammation. Male Wistar rats were divided into nine groups, the control group received distilled water orally for one week, while other groups were treated with ethanol to induce stomach ulcers, IR exposure, omeprazole, and different doses of ICME in combination with ethanol and/or IR. The study conducted comprehensive analyses, including LC-HRESI-MS/MS, to characterize the phenolic contents of ICME. Additionally, the Nrf2/HO−1 pathway, oxidative stress parameters, gastric pH, and histopathological changes were examined. The results showed that rats treated with IR and/or ethanol exhibited histopathological alterations, increased lipid peroxidation, decreased antioxidant enzyme activity, and reduced expression levels of Nrf2 and HO−1. However, pretreatment with ICME significantly improved these parameters. Phytochemical analysis identified 39 compounds in ICME, with flavonoids, hydroxybenzoic acids, and fatty acids as the predominant compounds. Virtual screening and molecular dynamics simulations suggested that ICME may protect against gastric ulceration by inhibiting oxidative stress and inflammatory mediators. In conclusion, this study demonstrates the potential of ICME as a natural gastroprotective therapy for preventing gastric ulcers. These findings contribute to the development of novel interventions for gastrointestinal disorders using natural plant extracts particularly in individuals with a history of radiation exposure.

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Section: Discussionmentioning

confidence: 99%

Ipomoea carnea mitigates ethanol-induced ulcers in irradiated rats via Nrf2/HO−1 pathway: an in vivo and in silico study

Ghareeb,

Mohammed,

Aboushousha

et al. 2024

Sci Rep

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“…This observation is consistent with that of Mai et al, who demonstrated that the water extract of domesticated Amauroderma rugosum effectively diminishes inflammation by inhibiting the protein expression of the NLRP3 inflammasome. Additionally, Selim et al reported the significant role of proinflammatory cytokines directly released by the NLRP3 inflammasome, namely IL-1β and IL-18, in the pathogenesis of gastric ulcers. Upon activation of the NLRP3 inflammasome, the subsequent liberation of IL-1β and IL-18 can stimulate inflammatory cells and trigger the release of further inflammatory mediators.…”

Section: Discussionmentioning

confidence: 99%

Atractylenolide I Alleviates Indomethacin-Induced Gastric Ulcers in Rats by Inhibiting NLRP3 Inflammasome Activation

Yuan,

Yu,

Sun

et al. 2024

J. Agric. Food Chem.

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“…Therefore, the exploration of food compounds, particularly natural food additives such as dyes, is an alternative approach to eliminate toxic synthetic food additives, promote healthy food, and prevent various health disorders [6,[46][47][48][49][50]. It is well-established that ethanol ingestion induces inflammatory reactions in the gastric mucosa, as evidenced by the induction of inflammatory genes and enzymes, epithelial cell necrosis, and increased gastric permeability [6,[46][47][48][49][50].The present study demonstrated that the consumption of ethanol leads to the degradation of purines, resulting in an excessive production of reactive oxygen species (ROS), which are known to mediate oxidative stress. This oxidative stress triggers the migration of neutrophils towards the damaged area of the gastric tissue.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of betanin against experimental gastric ulcer by reduction of ROS and suppression of inflammatory genes via NF-κB, iNOS, COX-2 and TNF-α pathways

Alghamdi

2023

JCNB

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Betanin, a prominent compound found in beetroot, however, the potential protective effects of this compound against gastric damage and ulceration have yet to be explored. This study aims to investigate the impact of purified beetroot betanin (Bet) on the activities of inflammatory enzymes and gene expressions associated with inflammation in gastric tissues. Gastric ulcer rats were induced by ethanol at dose 5ml/kg body weight. Ulcerated rats were treated by purified betanin or omeprazole; from which some inflammation-related genes and gastric-inflammation enzymes were investigated using RT-PCR and biochemical analysis, respectively. Bet effectively suppressed the activities of key enzymes involved in gastric mucosal inflammation, including 5-Lipoxygenase (5-LO), Hyaluronidase (HAase), and myeloperoxidase (MPO), by 58%, 50%, and 45%, respectively. Docking studies showed Bet binding to catalytic sites or key regions for enzymes’ activities, thus explaining the inhibitory capacity. Bet ingestion decreased the expression levels of inflammation-related genes, factor-kappa B (NF-ϰB) by 57%. This down-regulation subsequently led to a reduction in the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumour necrosis factor-α (TNF-α). Bet ingestion supressed thiobarbituric acid reactive substance (TBARS) rates by 59%, augmented nitric oxide (NO) level by 107% and protected gastric tissues from damage and ulceration. Bet revealed gastro-protective effects as confirmed by a reduction in the ulceration surface area and the acidity by 75.9% and 40%, respectively, and a significant increase in the weight of mucus and the curative index by 117% and 74.5%, respectively. In conclusion, these outcomes of physiological and molecular-based investigations are indicative of potential use of Bet as a functional food additive for the prevention of gastric ulcer.

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Fucoidan mitigates gastric ulcer injury through managing inflammation, oxidative stress, and NLRP3-mediated pyroptosis

Cited by 27 publications

References 51 publications

Ipomoea carnea mitigates ethanol-induced ulcers in irradiated rats via Nrf2/HO−1 pathway: an in vivo and in silico study

Ipomoea carnea mitigates ethanol-induced ulcers in irradiated rats via Nrf2/HO−1 pathway: an in vivo and in silico study

Atractylenolide I Alleviates Indomethacin-Induced Gastric Ulcers in Rats by Inhibiting NLRP3 Inflammasome Activation

The protective effects of betanin against experimental gastric ulcer by reduction of ROS and suppression of inflammatory genes via NF-κB, iNOS, COX-2 and TNF-α pathways

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