ArticleMarine drugs2011
Sulfated-polysaccharide fraction from red algae Gracilaria caudata protects mice gut against ethanol-induced damage.
Article in Marine drugs, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 52 citations in OpenAlex.
- Antioxidant and Cytoprotective Effects of Chilean Macroalgae Against Oxidative Stress-Induced Damage in Gastric Epithelial Cells.Nutrients · 2026Article
- Exploring the Therapeutic Potential of Green-Synthesized Gold Nanoparticles andAntioxidants (Basel, Switzerland) · 2024Article
- Targeting Host Sulphonyl Urea Receptor 2 Can Reduce Severity ofGastro hep advances · 2023Article
- Seaweed Supplementation Enhances Maximal Muscular Strength and Attenuates Resistance Exercise-Induced Oxidative Stress in Rats.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Gastroprotective Effects of Sulphated Polysaccharides from the Alga Caulerpa mexicana Reducing Ethanol-Induced Gastric Damage.Pharmaceuticals (Basel, Switzerland) · 2018Article
- Proteins and Carbohydrates from Red Seaweeds: Evidence for Beneficial Effects on Gut Function and Microbiota.Marine drugs · 2015Review
- A sulfated-polysaccharide fraction from seaweed Gracilaria birdiae prevents naproxen-induced gastrointestinal damage in rats.Marine drugs · 2012Article
- The role of hydrogen sulfide in gastric mucosal damage.Medical gas researchReview
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the gastroprotective activity of a sulfated-polysaccharide (PLS) fraction extracted from the marine red algae Gracilaria caudata and the mechanism underlying the gastroprotective activity. Male Swiss mice were treated with PLS (3, 10, 30 and 90 mg·kg(-1), p.o.), and after 30 min, they were administered 50% ethanol (0.5 mL/25 g(-1), p.o.). One hour later, gastric damage was measured using a planimeter. Samples of the stomach tissue were also obtained for histopathological assessment and for assays of glutathione (GSH) and malondialdehyde (MDA). Other groups were pretreated with l-NAME (10 mg·kg(-1), i.p.), dl-propargylglycine (PAG, 50 mg·kg(-1), p.o.) or glibenclamide (5 mg·kg(-1), i.p.). After 1 h, PLS (30 mg·kg(-1), p.o.) was administered. After 30 min, ethanol 50% was administered (0.5 mL/25 g(-1), p.o.), followed by sacrifice after 60 min. PLS prevented-ethanol-induced macroscopic and microscopic gastric injury in a dose-dependent manner. However, treatment with l-NAME or glibenclamide reversed this gastroprotective effect. Administration of propargylglycine did not influence the effect of PLS. Our results suggest that PLS has a protective effect against ethanol-induced gastric damage in mice via activation of the NO/K(ATP) pathway.
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