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Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury

Activation of the immune system in the central nervous system and oxidative stress play important roles in traumatic brain injury (TBI)-induced cognitive impairment. Rhamnetin possesses anti-inflammatory and anti-oxidative properties. This study aimed to detect the possible effects of rhamnetin on c...

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Detalles Bibliográficos
Autores principales: Zhang, Wei, Li, Ben, Guo, Yan, Bai, Yunan, Wang, Tongxin, Fu, Kun, Sun, Gaoling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Polish Society of Experimental and Clinical Immunology 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472538/
https://www.ncbi.nlm.nih.gov/pubmed/26155182
http://dx.doi.org/10.5114/ceji.2015.50831
Descripción
Sumario:Activation of the immune system in the central nervous system and oxidative stress play important roles in traumatic brain injury (TBI)-induced cognitive impairment. Rhamnetin possesses anti-inflammatory and anti-oxidative properties. This study aimed to detect the possible effects of rhamnetin on cognitive deficit, hippocampal inflammatory factors, and oxidative stress in rats with TBI. In this study, we established the traumatic brain injury model in rats. Rats respectively received vehicle saline or rhamnetin for 21 days. Cognitive functions were evaluated by assessing the acquisition of spatial learning and memory retention in Morris Water Maze test from day 15 to 19 post TBI. Levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor a (TNF-a), IL-10, and nuclear factor κB (NF-κB) in hippocampal homogenate were measured using ELISA. Oxidative stress was analysed by investigating the activities of MDA, H2O2, SOD, and GSH-Px. We found that rhamnetin significantly improved cognitive impairment in rats with TBI, and inhibited the inflammatory response and oxidative stress in the hippocampus. The results suggested that rhamnetin could enhance the recovery of cognitive deficits induced by TBI, and that its mechanism might be associated with the inhibition of inflammation and oxidative stress in the hippocampus.