Protective Effect of Dietary Polysaccharides from Yellow Passion Fruit Peel on DSS-Induced Colitis in Mice.

Inflammatory bowel disease (IBD) is a complex inflammatory disorder characterized by chronic and spontaneously relapsing inflammation of the gastrointestinal tract. IBD includes two idiopathic disorders: Crohn's disease (CD) and ulcerative colitis (UC). In particular, UC causes inflammation and ulceration of the colon and rectum. There is no cure for UC. The pharmacological treatment is aimed at controlling and/or reducing the inflammatory process and promoting disease remission. The present study investigated the possible protective effects of soluble dietary fiber (SDF) isolated from yellow passion fruit peel in the dextran sulfate sodium- (DSS-) induced colitis model in mice, induced by 5% of DSS. The animals were treated with SDF (10, 30, or 100 mg/kg (po)), and the disease activity index was monitored. Colon tissues were collected, measured, and prepared for oxidative stress, inflammation, and histology analysis. SDF improved body weight loss, colon length, and disease activity index and prevented colonic oxidative stress by regulating GSH levels and SOD activity. Furthermore, SDF reduced colonic MPO activity, TNF-α, and IL-1ß levels and increased IL-10 and IL-6 levels. As observed by histological analysis, SDF treatment preserved the colonic tissue, the mucus barrier, and reduced inflammatory cell infiltration. Although this is a preliminary study, taken together, our data indicate that SDF may improve the course of DSS-UC. More studies are needed to explore and understand how SDF promotes this protection.

Effects of the Crotalus durissus terrificus snake venom on hepatic metabolism and oxidative stress.

Snake venoms present different action mechanisms because of their complex composition, represented mainly by toxins and enzymes. This work aimed to investigate the effects of the Crotalus durissus terrificus(Cdt) venom in the liver. Wistar rats were inoculated intraperitoneally with saline (control) or Cdt venom. After 3, 4, or 6 h, the following parameters were analyzed: (a) hepatic function, (b) oxidative stress parameters, and (c) the metabolism of alanine in the isolated perfused liver. Plasma activities of alanine aminotransferase and aspartate aminotransferase and hepatic glutathione S-transferase and catalase presented significant elevation in rats inoculated with 300 µg ⋅ kg(-1) Cdt venom. Liver lipoperoxidation was enormously increased by venom doses of 100, 200, and 300 µg ⋅kg(-1) , whereas glutathione S-transferase was not changed. Perfused livers from rats inoculated with 1500 µg ⋅kg(-1) venom showed increased production of lactate, pyruvate, and ammonia when alanine was the metabolic substrate. These results demonstrate that the Cdt venom can produce several changes in hepatocytes. The causes of the changes are possibly related to the disequilibrium in the redox homeostasis but also to specific needs of the poisoned organism, for example, an increased supply of lactate and pyruvate in response to an increased activity of the Cori cycle.

Hepatic effects of flunixin-meglumin in LPS-induced sepsis.

The aim of this study was to evaluate the actions of the non-steroidal anti-inflammatory drug flunixin-meglumin (FM) on the changes caused by lipopolysaccharide (LPS)-induced sepsis in the rat liver. Eight groups of five adult male Wistar rats were analysed: (1) saline injected (controls), (2) FM treated with 1.1 mg/kg, (3) FM treated with 2.2 mg/kg, (4) LPS-injected (10 mg/kg), (5) LPS-injected with 1.1 mg/kg FM pretreatment, (6) LPS-injected with 2.2 mg/kg FM pretreatment, (7) LPS-injected with 1.1 mg/kg FM post-treatment and (8) LPS-injected with 2.2 mg/kg FM post-treatment. All drugs were intraperitoneally injected. The following parameters were evaluated: plasma levels of hepatic enzymes and urea, hepatic histological characteristics, antioxidant enzymes and several metabolic fluxes. The latter comprised gluconeogenesis, ureagenesis and oxygen consumption. Liver damage in LPS-induced sepsis was characterized by histological changes, increased plasma levels of alanine aminotransferase and aspartate aminotransferase (P < 0.001) and diminished gluconeogenesis (P < 0.001) and ureagenesis (P < 0.01). LPS also induced oxidative stress as evidenced by increased catalase (P < 0.05) and superoxide dismutase activities and enhanced lipid peroxidation (P < 0.001). Pretreatment of the animals with FM minimized the histological changes and normalized, in part, all enzymatic activities. Pretreatment of the animals with FM also normalized gluconeogenesis and partly restored ureagenesis (P < 0.05). These and other results show that LPS-induced sepsis may lead to severe liver damage, affecting both structure and function. Treatment with FM can be used to avoid this damage. The antioxidant properties of FM can be, partly at least, responsible for this protective action.