Sulfated-polysaccharide fraction extracted from red algae Gracilaria birdiae ameliorates trinitrobenzenesulfonic acid-induced colitis in rats.

OBJECTIVES: The aim of this study was to evaluate the protective effect of the sulfated-polysaccharide (PLS) fraction extracted from the seaweed Gracilaria birdiae in rats with trinitrobenzenesulfonic acid (TNBS)-induced colitis. METHODS: In the experiments involving TNBS-induced colitis, rats were pretreated with polysaccharide extracted from G. birdiae (PLS: 30, 60 and 90 mg/kg, 500 µL p.o.) or dexamethasone (control group: 1 mg/kg) once daily for 3 days starting before TNBS instillation (day 1). The rats were killed on the third day, the portion of distal colon was excised and washed with 0.9% saline and pinned onto a wax block for the evaluation of macroscopic scores. Samples of the intestinal tissue were used for histological evaluation and assays for glutathione (GSH) levels, malonyldialdehyde (MDA) concentration, myeloperoxidase (MPO) activity, nitrate and nitrite (NO3 /NO2 ) concentration and cytokines levels. KEY FINDINGS: PLS treatment reduced the macroscopic and microscopic TNBS-induced intestinal damage. Additionally, it avoided the consumption of GSH, decreased pro-inflammatory cytokine levels, MDA and NO3 /NO2 concentrations and diminished the MPO activity. CONCLUSIONS: Our results suggest that the PLS fraction has a protective effect against intestinal damage through mechanisms that involve the inhibition of inflammatory cell infiltration, cytokine releasing and lipid peroxidation.

Role of the NO/K ATP pathway in the protective effect of a sulfated-polysaccharide fraction from the algae Hypnea musciformis against ethanol-induced gastric damage in mice

Seaweeds are the most abundant source of polysaccharides such as alginates and agar, as well as carrageenans. This study aimed to investigate the gastroprotective activity and the mechanism underlying this activity of a sulfated-polysaccharide fraction extracted from the algae Hypnea musciformis (Wulfen) J.V. Lamour. (Gigartinales-Rhodophyta). Mice were treated with sulfated-polysaccharide fraction (3, 10, 30, and 90 mg/kg, p.o.) and, after 30 min, they were administered 50% ethanol (0.5 mL/25 g, p.o.). After 1 h, gastric damage was measured using a planimeter. In addition, samples of the stomach tissue were obtained for histopathological examination and for assays to determine the glutathione and malondialdehyde levels. Other groups of mice were pretreated with N G-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.p.), aminoguanidine (100 mg/kg, i.p.), or glibenclamide (10 mg/kg, i.p.). After 30 min to the aminoguanidine group and 1 h to the other groups, sulfated-polysaccharide fraction (30 mg/kg, p.o.) was administered and gastric damage was induced as described above. Sulfated-polysaccharide fraction prevented ethanol-induced gastric injury in a dose-dependent manner. However, treatment with L-NAME or glibenclamide reversed this gastroprotective effect. Administration of aminoguanidine did not influence the effect of sulfated-polysaccharide fraction. Our results suggest that sulfated-polysaccharide fraction exerts a protective effect against ethanol-induced gastric damage via activation of the NO/K ATP pathway.

A sulfated-polysaccharide fraction from seaweed Gracilaria birdiae prevents naproxen-induced gastrointestinal damage in rats.

Red seaweeds synthesize a great variety of sulfated galactans. Sulfated polysaccharides (PLSs) from seaweed are comprised of substances with pharmaceutical and biomedical potential. The aim of the present study was to evaluate the protective effect of the PLS fraction extracted from the seaweed Gracilaria birdiae in rats with naproxen-induced gastrointestinal damage. Male Wistar rats were pretreated with 0.5% carboxymethylcellulose (control group-vehicle) or PLS (10, 30, and 90 mg/kg, p.o.) twice daily (at 09:00 and 21:00) for 2 days. After 1 h, naproxen (80 mg/kg, p.o.) was administered. The rats were killed on day two, 4 h after naproxen treatment. The stomachs were promptly excised, opened along the greater curvature, and measured using digital calipers. Furthermore, the guts of the animals were removed, and a 5-cm portion of the small intestine (jejunum and ileum) was used for the evaluation of macroscopic scores. Samples of the stomach and the small intestine were used for histological evaluation, morphometric analysis and in assays for glutathione (GSH) levels, malonyldialdehyde (MDA) concentration, and myeloperoxidase (MPO) activity. PLS treatment reduced the macroscopic and microscopic naproxen-induced gastrointestinal damage in a dose-dependent manner. Our results suggest that the PLS fraction has a protective effect against gastrointestinal damage through mechanisms that involve the inhibition of inflammatory cell infiltration and lipid peroxidation.