الفهرس | Only 14 pages are availabe for public view |
Abstract The new millennium has witnessed the emergence of a modern epidemic, the metabolic syndrome (MS), in approximately 25% of the world{u2019}s adult population. The current study aimed to investigate the effect of the TNF-Ü antagonist infliximab on fructose-induced MS in rats. Rats were administered fructose (10%) in drinking water for 12 weeks to induce the experimental MS model. Adult male Sprague Dawley rats (150-200g) were divided into control and MS groups, The later was subdivided after 12 weeks into two groups namely MS control and infliximab (5mg/kg) group. The drug was injected once weekly intraperitoneally starting on the 13th week for 4 weeks. Increase in body weight, blood glucose level, serum triglycerides (TGs), and blood pressure were present in MS rats. They also prompted increases in serum levels of leptin, TNF-Ü, and oxidative stress markers. Treatment with infliximab did not affect body weight, hyperglycemia or hypertension, but decreased serum TGs. Infliximab also increased serum superoxide dismutase (SOD) and glutathione peroxidase (Gpx) activities. Surprisingly, infliximab increased malonedialdehyde (MDA) above the value of MS. These results reflect the fact that infliximab affects the manifestations of MS in rats. Though infliximab reduced TGs and increased antioxidant enzymes, the drug failed to combat MS-mediated obesity, hyperglycemia, hypertension, and elevated MDA above the insult |