Résumé
Objective:To evaluate the relationship between early postoperative cognitive dysfunction and neuromodulator protein 1β(NRG1β) in aged rats.Methods:Pathogen-free healthy male Sprague-Dawley rats, aged 18-20 months, weighing 600-700 g, were divided into 3 groups ( n=10 each) using a random number table method: control group (group C), operation group (group O) and NRG1β group (group N). Exploratory laparotomy was performed in group O and group N. NRG1β 0.5 μg/kg was slowly injected into the lateral ventricle on 1 day before surgery in group N, while the equal volume of 0.1 mol/L phosphate buffer solution was given instead in C and O groups.Learning and memory function was assessed using Morris water maze test performed at day 3 after operation.The rats were then sacrificed, and the hippocampi were removed for determination of the expression of nuclear factor kappa B (NF-κB) p65 (by Western blot) and contents of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) (by enzyme-linked immunosorbent assay). Results:Compared with group C, the postoperative escape latency was significantly prolonged, the expression of NF-κB p65 was up-regulated, and the contents of IL-1β and TNF-α were increased in group O and group N ( P<0.05). Compared with group O, the postoperative escape latency was significantly shortened, the expression of NF-κB p65 was down-regulated, and the contents of IL-1β and TNF-α were decreased in group N ( P<0.05). Conclusion:NRG1β is involved in the endogenous protective mechanism of early postoperative cognitive dysfunction probably by inhibiting the activation of NF-κB pathway and inhibiting inflammatory responses in aged rats.
Résumé
Objective To investigate the effects and mechanisms of propofol and dexmedetomidine on neurites and synapses of hippocampal neurons neonatal rats, in vitro. Methods Hippocampal neurons of neonatal Sprague-Dawley rats were cultured 6 days, in vitro and were divided into control group (Group C), solvent of propofol group (Group S), propofol group (Group P), dexmedetomidine group (Group D),propofol and dexmedetomidine group (Group PD), and yohimbine group (Group Y). All groups were cultured for 24 h further. Neuron morphology and the expression of protein were measured. Results After exposing to propofol, we found that the mean total length of neurites of primary cultured hippocampal neurons and synapses and the expression of BDNF, TrkB and CRMP-2 protein were reduced; dexmedetomidine played a protective role. Moreover, yohimbine, partly inhibited neuroprotection of dexmedetomidine. Conclusions Propofol decreases the development of neurites and synapses of hippocampal neurons neonatal rats, in vitro, and dexmedetomidine provides a protective effect on propofol by up-regulating the expression of BDNF, TrkB and CRMP-2. The effect, partly has a concern aboutα2-adrenergic agonist.