Abstract
Objective To evaluate the role of Wnt/β-catenin signaling pathway in lithium chloride preconditioning-induced improvement in postoperative cognitive function of aged rats. Methods A total of 100 pathogen-free healthy male Sprague-Dawley rats, aged 18 months, weighing 540-650 g, were divided into 5 groups(n=20 each)using a random number table: control group(group C), surgery group(group S), lithium chloride preconditioning group(group L), secreted frizzled-related protein 1(sFRP-1) group(group F)and lithium chloride preconditioning plus sFRP-1 group(group L+ F). Lithium chloride 2 mmol/kg was intraperitoneally injected once a day for 5 consecutive days before operation in L and L+ F groups.In F and L + F groups, sFRP-1 10 μl(concentration 10 μg/ml)was injected into the ventricle at 1 day before operation.Ten rats in each group were randomly sacrificed at 1 day after operation, and the hippocampi were removed for determination of the expression of phosphorylated glycogen synthase kinase-3 beta(p-GSK-3β), β-catenin and Wnt in hippocampal tissues(by Western blot). The rest rats underwent Morris water maze test at day 3-7 after operation, and the concentrations of amyloid beta 42(Aβ-42)and phosphorylated tau-181 protein(p-tau-181)in cerebrospinal fluid(CSF)were detected by enzyme-linked immunosorbent assay at day 7 after operation. Results Compared with group C, the escape latency was significantly prolonged at 3-7 days after operation, and the concentration of Aβ-42 in CSF was increased in the other four groups, and the expression of Wnt, p-GSK-3β and β-catenin in hippocampal tissues was down-regulated in group S, the expression of Wnt, p-GSK-3β and β-catenin in hippocampal tissues was significantly up-regulated in L and L+ F groups, and the concentration of p-tau-181 in CSF was significantly increased in S and L+ F groups(P<0.05). Compared with group S, the escape latency was significantly shortened at 3-7 days after operation in group L and at 5-7 days after operation in group L+ F, and the expression of Wnt, p-GSK-3β and β-catenin was significantly up-regulated, and the concentrations of Aβ-42 and p-tau-181 in CSF were decreased in L and L+ F groups(P<0.05). Compared with group L, the escape latency was significantly prolonged at 3-6 days after operation, the expression of Wnt, p-GSK-3β and β-catenin was down-regulated, and the concentration of p-tau-181 in CSF was increased in group L+ F(P<0.05). Compared with group F, the escape latency was significantly shortened at 3-7 days after operation, the expression of Wnt, p-GSK-3β and β-catenin was up-regulated, and the concentrations of Aβ-42 and p-tau-181 in CSF were decreased in group L+ F(P<0.05). Conclusion The mechanism by which lithium chloride preconditioning improves in postoperative cognitive function is partially related to activating Wnt/β-catenin signaling pathway in aged rats. Key words: Lithium chloride; Wnt proteins; Aged; Cognition disorders; Preconditioning
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