Abstract

The aim of the present study was to demonstrate the antiulcer activity and mechanism of bezafibrate in a rat model of aspirin-induced gastric ulcer. We used an aspirin-induced gastric ulcer model. Bezafibrate was administered orally in graded doses (10 mg/kg, 25 mg/kg, 50 mg/kg, 100 mg/kg, and 200 mg/kg) to detect the best effective antiulcer dose of bezafibrate. The parameters measured were: ulcer index, histopathological scoring of gastric ulcer, gastric juice analysis, gastric mucosal lipid peroxidation parameters, estimation of NO metabolite in blood, mRNA expression of inducible NO synthase iNOS and constitutive NO synthase (cNOS) in gastric mucosa, and gastric mucosal DNA fragmentation. The dose-dependent antiulcer activity of bezafibrate was shown by the ulcer index and histopathological score. Bezafibrate (100 mg/kg) significantly reduced total acidity, free acidity, and pepsin activity, and increased total hexoses and total proteins. Bezafibrate (100 mg/kg) also significantly reduced lipid peroxidation, inhibited iNOS expression, preserved cNOS expression, and inhibited DNA fragmentation. Bezafibrate can decrease aspirin-induced gastric mucosal injury via reducing lipid peroxidation, inhibiting iNOS expression, preserving cNOS expression, and decreasing DNA fragmentation.

Abstract

The aim of this experimental study is to evaluate the efficacy of a novel intraarticular drug in a papain induced osteoarthritis (OA) rat model and compare with the traditional hyaluronat (HA) visco supplementation. An early stage OA model was induced by the intra-articular injection of papain enzyme in the right knee joints of 44 Sprague-Dawley rats. Eleven rats (eleven right knees: papain group, 11 left knees: control group) were chosen randomly 28 days after the last injection and sacrificed for verifying OA. The remaining rats (n = 33) were randomly divided into 3 groups. Group 1 was injected 0, 2 mL of sterile saline solution (0, 9%), group 2 was injected 0, 2 mL HA and the group 3 was injected 0, 2 mL of HA-CSNAG (hyaluronat, chondritin sulfate, N-acetyl-d -glucosamine) combination in the right knees. Injections were performed on the 35th, the 42nd and the 49th days consecutively. Two weeks after the last injection, all groups were sacrificed to evaluate the severity of OA according to Mankin system. Early stage of OA was verified regarding total Mankin scores (p < 0.05). There was statistically significant difference between Group 1 and Group 2 (p < 0.05), between Group 1 and Group 3 (p < 0.05) on the 63th day regarding total Mankin scores. Group 3 showed statistically significant improvement in terms of proteoglycan content of matrix when compared to Group 2 (p < 0, 05). HA-CS-NAG compound in hydrogel form is more chondroprotective to rats' cartilage when compared to HA during the early stages of OA.

Abstract

Use of pecan shell fiber in human food is presently limited, but could increase pending demonstration of safety. In a 91-day rat study, pecan shell fiber was administered at dietary concentrations of 0 (control), 50 000, 100 000 or 150 000 ppm. There was no effect of the ingredient on body weight of males or females or food consumption of females. Statistically significant increases in food consumption were observed throughout the study in 100 000 and 150 000 ppm males, resulting in intermittent decreases in food efficiency (150 000 ppm males only) that were not biologically relevant. All animals survived and no adverse clinical signs or functional changes were attributable to the test material. There were no toxicologically relevant changes in hematology, clinical chemistry or urinalysis parameters or organ weights in rats ingesting pecan shell fiber. Any macroscopic or microscopic findings were incidental, of normal variation and/or of minimal magnitude for test substance association. Pecan shell fiber was non-mutagenic in a bacterial reverse mutation test and non-clastogenic in a mouse peripheral blood micronucleus test. Based on these results, pecan shell fiber has an oral subchronic (13-week) no observable adverse effect level (NOAEL) of 150 000 ppm in rats and is not genotoxic at the doses analyzed.