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/25g⁻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.

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.

This study aimed to evaluate the effect of Lactobacillus reuteri DSM 17938 (DSM) on ethanol-induced gastric injury, and if its possible mechanism of action is related to inhibiting the transient receptor potential vanilloid type 1 (TRPV1). We evaluated the effect of supplementing 10⁸ CFU•g body wt⁻¹•day⁻¹ of DSM on ethanol-induced gastric injury. DSM significantly reduced the ulcer area (1.940 ± 1.121 mm²) with 3 days of pretreatment. The effects of DSM supplementation were reversed by Resiniferatoxin (RTX), TRPV1 agonist (3 nmol/kg p.o.). Substance P (SP) (1 μmol/L per 20 g) plus 50% ethanol resulted in hemorrhagic lesions, and DSM supplementation did not reverse the lesion area induced by administering SP. TRPV1 staining intensity was lower, SP, malondialdehyde (MDA) and nitrite levels were reduced, and restored normal levels of antioxidant parameters (glutathione and superoxide dismutase) in the gastric mucosa in mice treated with DSM. In conclusion, DSM exhibited gastroprotective activity through decreased expression of TRPV1 receptor and decreasing SP levels, with a consequent reduction of oxidative stress.

5-Fluorouracil (5-FU) is an antimetabolite widely prescribed in cancer treatments, but its use in highly proliferative tissues can cause significant problems such as mucositis. Bacillus clausii is a probiotic commonly used for protection against acute diarrhea, gastrointestinal dysbiosis and inflammatory bowel diseases. We investigated the effect of B. clausii on 5-FU intestinal mucositis in mice. B. clausii was administered concomitantly with 5-FU on the first day and alone for the other two days. After the third day of 5-FU (450 mg/kg, ip), the animals were euthanized. Ileum samples were removed for evaluation for histopathological and biochemical analyses (myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA), catalase (CAT), interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α). In addition, we investigated gastric emptying and intestinal transit, intestinal permeability, intestinal smooth muscle contractility, transepithelial electrical resistance and intestinal transport of water and electrolytes. B. clausii reduced histopathological scores and increased the villus/crypt ratio in all intestinal segments after mucositis. B. clausii attenuated 5-FU-induced weight loss. The probiotic treatment increased GSH levels, reduced MPO and CAT activity, and also reduced MDA, IL-1β and TNF-α levels. B. clausii attenuated the delay in gastric emptying, water and electrolyte secretion and intestinal hypercontractility, and increased 5-FU-induced intestinal permeability. Thus, our data suggest that B. clausii may be a potential candidate for the treatment of chemotherapy-induced intestinal mucositis.