dinoprost and Inflammatory-Bowel-Diseases

Iron deficiency is a common complication of inflammatory bowel disease. Oral iron therapy may reinforce intestinal tissue injury by catalyzing production of reactive oxygen species.. To compare the effects of ferrous sulphate and non-ionic iron-polymaltose complex on markers of oxidative tissue damage and clinical disease activity in patients with inflammatory bowel disease.. Forty-one patients with inflammatory bowel disease and iron deficiency were randomized to treatment with ferrous sulphate 100 mg twice a day or iron-polymaltose complex 200 mg once a day for 14 days.. Following ferrous sulphate, plasma malondialdehyde increased (P = 0.02), while urine 8-isoprostaglandin F(2alpha) and plasma antioxidants did not change significantly. Iron-polymaltose complex did not change plasma malondialdehyde, urine 8-isoprostaglandin F(2alpha) or plasma antioxidants. Comparing the two treatments, changes in plasma malondialdehyde tended to differ (P = 0.08), while urine 8-isoprostaglandin F(2alpha) and plasma antioxidants did not differ. Neither ferrous sulphate nor iron-polymaltose complex altered clinical disease activity indices.. Ferrous sulphate increased plasma malondialdehyde, a marker of lipid peroxidation. Comparing treatment with ferrous sulphate and iron-polymaltose complex, changes in plasma malondialdehyde tended to differ. Clinical disease activity was unchanged after both treatments.

Topics: Adolescent; Adult; Aged; Antioxidants; Biomarkers; Dinoprost; Female; Ferric Compounds; Ferrous Compounds; Hematinics; Humans; Inflammatory Bowel Diseases; Iron Deficiencies; Male; Malondialdehyde; Middle Aged; Oxidation-Reduction; Oxidative Stress; Prospective Studies; Reactive Oxygen Species; Tablets; Vasoconstrictor Agents

Harpagophytum procumbens has a long story of use for the treatment of inflammatory diseases. Considering both the antiinflammatory effects of H. procumbens in multiple tissues and the stability of harpagoside in artificial intestinal fluid, the aim of the present study was to explore the possible protective role of a microwave-assisted aqueous Harpagophytum extract (1-1000 μg/mL) on mouse myoblast C2C12 and human colorectal adenocarcinoma HCT116 cell lines, and isolated rat colon specimens challenged with lipopolysaccharide (LPS), a validated ex vivo model of acute ulcerative colitis. In this context, we evaluated the effects on C2C12 and HCT116 viability, and on LPS-induced production of serotonin (5-HT), tumor necrosis factor (TNF)-α, prostaglandin (PG)E

Topics: Animals; Cell Line, Tumor; Colon; Dinoprost; Dinoprostone; Glycosides; Harpagophytum; Humans; Inflammatory Bowel Diseases; Lipopolysaccharides; Male; Mice; Oxidative Stress; Plant Extracts; Plant Roots; Pyrans; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha