ABSTRACT
Inflammation is a protective biological reaction against infection and has undesirable effects. Although bergenin (BG),a C-glycoside derivative of 4-O-methyl gallic acid, has many pharmacological properties, no study has demonstratedthe activity of BG in inflammatory mediators, such as histamine and prostaglandin E2 (PGE2). The present studyinvestigated the anti-inflammatory activity of BG obtained from Peltophorum dubium Taub, in edema models inducedby carrageenan and inflammatory mediators in Swiss mice. The assessment of its toxicity was also conducted. Theevaluations of this study indicated that the pre-treatment with BG (25 mg/kg) significantly reduced edema induced bycarrageenan, compound 48/80, histamine, and PGE2 (p < 0.05). Also, pre-treatment with BG inhibited the recruitmentof leukocytes and neutrophils, reducing adhesion and rolling of these cells, myeloperoxidase (MPO) activity,malondialdehyde (MDA) levels, and vascular permeability. Treatment with BG (2,000 mg/kg) showed no toxicsigns in hippocratic screening, weight of animals, water and feed intake, vital organs weight and histopathologicalevaluation, and hematological and biochemical parameters. In conclusion, these results show that the BG obtainedfrom P. dubium Taub has anti-inflammatory activity against different models of inflammation, reducing neutrophilmigration and damage caused by oxidative stress and lipid peroxidation. BG did not present toxic effects in theevaluated parameters.
ABSTRACT
AbstractSome publications have described the pharmacological properties of latices proteins. Thus, in the present study proteins from Plumeria pudica Jacq., Apocynaceae, latex were evaluated for anti-inflammatory and antinociceptive activities. Obtained data showed that an intraperitoneal administration of different doses of latex was able to reduce the paw edema induced by carrageenan in a dose-dependent manner (better dose 40 mg/kg; 72.7% inhibition at 3rd and 78.7% at 4th hour) and the edema induced by dextran (40 mg/kg; 51.5% inhibition at 30 min and 93.0% at 1st hour). Inhibition of edema induced by carrageenan was accompanied by a reduction of myeloperoxidase activity. Pre-treating animals with latex (40 mg/kg) also inhibited the paw edema induced by histamine, serotonin, bradykinin, prostaglandin E2, compound 48/80. Additionally, the latex (40 mg/kg) reduced the leukocyte peritoneal migration induced by carrageenan and this event was followed by reduction of IL-1β and TNF-α in peritoneal fluid. The latex-treatment (40 mg/kg) reduced the animal abdominal constrictions induced by acetic acid and the first phase on paw licking model induced by formalin. When latex was treated with heat (at 100 °C for 30 min), anti-edematogenic and myeloperoxidase activities were significantly reduced, indicating the involvement of heat-sensitive proteins on anti-inflammatory effect. Our results evidence that latex fluids are a source of proteins with pharmacological properties.
ABSTRACT
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.