Propofol improves brain injury induced by chronic cerebral hypoperfusion in rats.

Abstract

To study effect of propofol on cognitive dysfunction and brain injury in a rat model of chronic cerebral hypoperfusion. The bilateral carotid artery ligation (bilateral common carotid artery occlusion and BCCAO) to establish rat model of chronic cerebral hypoperfusion and randomly assigned to 4 groups (n = 10): sham‐operation group treated with saline model group, propofol treatment model group, normal saline treatment, propofol treatment in the sham‐operation group; continuous intraperitoneal injection of propofol and saline for 12 weeks. Morris water maze was used to evaluate the learning and memory ability of rats. Determination of central cholinergic and oxidative stress in brain tissue by spectrophotometry. Detection of inflammatory response in brain tissue by immunohistochemistry and ELISA method. Detection of neuronal loss in brain tissue by Nissl and TUNEL staining. Compared with the saline‐treated model group, propofol in model group significantly increased the rat brain tissue SOD activity (p < .01) and GPX activity (p < .01), decreased the MDA levels (p < .01) and protein carbonyl compound levels (p < .01). The propofol treatment of model group rats hippocampal GFAP‐immunoreactive satellite glial cells (p < .01) and immune Iba1‐positive microglia cells (p < .01) area percent compared to saline‐treated model group decreased significantly. The number of normal propofol treatment of model group rats hippocampus neuron than in physiological saline treatment model group rats was significantly increased (p < .01). Propofol can improve chronic cerebral hypoperfusion in rats induced by cognitive dysfunction and brain damage.