Weekend warrior exercise model for protection from chronic mild stress­induced depression and ongoing cognitive impairment.

We aim to investigate the role and biological mechanisms of the weekend warrior (WW) exercise model on depression­induced rats in comparison to the continuous exercise (CE) model. Sedentary, WW, and CE rats were subjected to chronic mild stress (CMS) procedure. CMS and exercise protocols continued for six weeks. Anhedonia was evaluated by sucrose preference, depressive behavior by Porsolt, cognitive functions by object recognition and passive avoidance, and anxiety levels by open field and elevated plus maze. After behavioral assessments, brain tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, superoxide dismutase and catalase activities and GSH content, tumor necrosis factor­α (TNF­α), interleukin­6 (IL­6), IL­1ß, cortisol and brain­derived neurotrophic factor levels and histological damage was assessed. CMS­induced depression­like outcomes with increases in anhedonia and decreases in cognitive measures that are rescued with both exercise models. The increased immobilization time in the Porsolt test was decreased with only WW. Exercise also normalized the suppression of antioxidant capacity and MPO increase induced by CMS in both exercise models. MDA levels also declined with both exercise models. Anxiety­like behavior, cortisol levels, and histological damage scores were exacerbated with depression and improved by both exercise models. TNF­α levels were depleted with both exercise models, and IL­6 only with WW. WW was as protective as CE in CMS­induced depression­like cognitive and behavioral changes via suppressing inflammatory processes and improving antioxidant capacity.

Neuropeptide W Attenuates Oxidative Multi-Organ Injury in Rats Induced with Intra-Abdominal Sepsis.

Sepsis leads to systemic hypotension, disturbed perfusion, inflammation, and tissue toxicity in vital organs. Neuropeptide W (NPW) has modulatory effects in the control of blood pressure and inflammatory processes, implicating a potential beneficial effect against sepsis-induced oxidative damage. Under anesthesia, male Sprague Dawley rats underwent cecal ligation and puncture. Immediately after surgery, either saline or TNF-alpha inhibitor (etanercept; 1 mg/kg) antibiotic (ceftriaxon; 10 mg/kg) combination or NPW (0.1, 1, or 3 µg/kg) was given subcutaneously, and injections were repeated on the 12th and 24th h. The sham-operated control group was treated with saline at the same time points. All rats were euthanized on the 25th h of surgery. Sepsis resulted in oxidative damage of the brain, heart, lung, liver, and kidney. Elevations in blood urea nitrogen and alkaline phosphatase, showing renal and hepatic dysfunction, were not evident when septic rats were treated with NPW. NPW reduced serum levels of C-reactive protein, corticosterone, and interleukin-6, while histopathologically verified tissue damage in all the studied tissues was ameliorated. NPW treatment suppressed lipid peroxidation in the heart, lung, and brain, and the depleted antioxidant GSH levels of the brain and heart were replenished by NPW. Moreover, sepsis-related neutrophil recruitment to the liver and lung was also suppressed by NPW. Although the survival rate of the rats was not significantly prolonged by NPW, most of these improvements in systemic and local inflammatory events were comparable with those reached by the etanercept and antibiotic combination, suggesting the therapeutic impact of NPW during the acute period of sepsis.