orabase and Reperfusion-Injury

Topics: Animals; Antioxidants; Apoptosis; Carboxymethylcellulose Sodium; Catalase; Collagen; Drug Carriers; Drug Delivery Systems; Endothelial Cells; Humans; Hydrogen Peroxide; Inflammation; Interleukin-10; Oxidative Stress; Peptides; Rats; Reactive Oxygen Species; Reperfusion Injury; Retina

Oleanolic acid (OA) has been used to treat liver disorders, but whether it can attenuate hepatic ischemia-reperfusion- (IR-) associated liver dysfunction remains unexplored. In the present study, 160 male Sprague-Dawley rats were equally divided into five groups: group SH received neither hepatic IR nor drugs; group IR received hepatic IR without drugs; group CM and group OA received 0.5% sodium carboxymethylcellulose and 100 mg/kg OA, intragastrically, once a day for seven days before the hepatic IR, respectively; on the basis of treatment in group OA, group OA+wortmannin further received 15 μg/kg of PI3K inhibitor wortmannin, intraperitoneally, 30 min before the hepatic IR. Then each group was equally divided into four subgroups according to four time points (preoperation, 0 h, 3 h, and 6 h after reperfusion). Serum ALT activity, IL-1β concentration, and hepatic phosphorylation of PI3K, Akt, and GSK-3β protein expression were serially studied. We found that OA pretreatment improved histological status and decreased serum ALT and IL-1β levels. It also increased p-PI3K, p-Akt, and p-GSK-3β protein expression at all the four time points. Prophylactic wortmannin partially reversed OA's protective effects. The data indicate that OA pretreatment protects liver from IR injury during the acute phase partially through PI3K/Akt-mediated inactivation of GSK-3β.

Topics: Androstadienes; Animals; Blotting, Western; Carboxymethylcellulose Sodium; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Interleukin-1beta; Liver; Male; Oleanolic Acid; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Wortmannin

Treatments addressing variously theorised pathophysiological mechanisms of small intestinal adhesions have been reported. This study applied those classes of treatments to the most clinically relevant aetiology of post operative adhesions.. Treatments addressing the pathophysiology of ischaemia-reperfusion induced adhesions would accordingly reduce the incidence of adhesions from this model.. Four classes of treatments were administered for 72 h to 16 foals subjected to complete ischaemia followed by reperfusion to create peritoneal adhesions. These groups were: 1) FPG group--flunixin meglumine (1.1 mg/kg bwt i.v., divided q.i.d.), potassium penicillin G (22,000 iu/kg bwt i.v., q.i.d.) and gentamicin (2.2 mg/kg bwt i.v., t.i.d.); 2) HEP group--heparin (80 iu/kg bwt subcut., b.i.d.); 3) DMSO group--dimethylsulphoxide (DMSO) (20 mg/kg bwt [diluted in 500 ml normal saline] i.v., b.i.d.); and 4) SCMC group--sodium carboxymethylcellulose (500 ml 3% sterile solution intraperitoneally, administered only at the beginning of surgery).. Post operative intestinal obstruction did not occur in any foal. After 10 days, necropsy revealed bowel-to-bowel adhesions in none of the FPG or DMSO groups, in 2/4 of the SCMC group, in 3/4 of the HEP group and 5/6 foals subjected to the procedure without treatment (UIR group).. Inhibition of the inflammation associated with ischaemia and reperfusion in foals treated with FPG or DMSO decreased small intestinal adhesions in foals.. Although anti-inflammatory therapy was shown to eliminate bowel-bowel adhesions in this controlled study, it must be remembered that clinical cases are without control. These therapies are advised to improve the result but are unlikely to eliminate the problem.

Topics: Animals; Animals, Newborn; Anti-Bacterial Agents; Carboxymethylcellulose Sodium; Dimethyl Sulfoxide; Heparin; Horse Diseases; Horses; Intestinal Diseases; Intestine, Small; Ischemia; Peritoneal Diseases; Peritoneum; Postoperative Complications; Random Allocation; Reperfusion Injury; Tissue Adhesions