Adiponectin and Traumatic Brain Injury
Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke
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Abstract Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin. Adult male Sprague–Dawley rats were subjected to lateral fluid percussion injury using the Dragonfly device. Immunohistochemical studies showed that the adiponectin expression was increased in the cerebral cortex at 24 h after injury and in the hippocampus at 72 h after injury. Our findings suggest that adiponectin might participate in the pathophysiological process occurring after traumatic brain injury. Keywords Adiponectin • Traumatic brain injury • Lateral fluid percussion • Rat
Introduction Adiponectin is a hormone secreted exclusively by adipose tissue, and plays an important role in the regulation of tissue inflammation and insulin sensitivity [10, 11]. Because of the effects it has, adiponectin is described as an anti-diabetic and anti-atherogenic adipokine [3]. Additionally, recent experimental studies using a cerebral ischemia–reperfusion model have shown that high levels of adiponectin were detected in the ischemic hemisphere [12], and that adiponectin may exert a cerebroprotective action [7]. However, little is known
S. Takeuchi (*), K. Wada, H. Nawashiro, Y. Uozumi, N. Otani, H. Osada, K. Nagatani, H. Kobayashi, T. Suzuki, and K. Shima Department of Neurosurgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan e-mail: [email protected]
about the effects of adiponectin on traumatic brain injury (TBI). The aim of the present study was to examine the changes in the plasma adiponectin levels and the expression of adiponectin in the brain after TBI.
Materials and Methods Animals and Experimental Procedures All experimental procedures were approved by the Animal Care and Use Committee of the National Defense Medical College. Sprague–Dawley rats (male, 300–400 g in weight; 9–10 weeks of age) were used for the study. The rats were housed in individual cages under controlled environmental conditions (12/12 h light/dark cycle, 20–22 °C; room temperature) with food and water freely available, for 1 week before the experimental surgery. The rats were anesthetized with isofluorane (1.5 %) in a 30 % oxygen to 70 % nitrous oxide gas mixture via a nose cone and were fixed in a stereotaxic frame for the procedure. A 4.8-mm craniotomy was made over the right parietal cortex (3.8 mm posterior and 2.5 mm lateral to the bregma), keeping the underlying dura intact. A plastic Luer Lock was placed over the opening and secured with dental acrylic cement. The rats were returned to their cages and allowed free access to water overnight. The following day, the rats were anesthetized, intubated, and maintained on a mechanical ventilator after infusion of pancronium bromide
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