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Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

机译:氯化锂改善七氟醚麻醉在大鼠中诱导的认知功能障碍

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Postoperative cognitive dysfunction is a common complication in elderly patients after surgeries involving anesthesia, but the underlying mechanisms are poorly understood. Lithium is a conventional treatment for bipolar disorder, which exerts a neuroprotective role in various diseases by inhibiting glycogen synthase kinase‐3β (GSK‐3β) in the brain and spinal cord. However, it is not known whether lithium chloride (LiCl) can protect against cognitive dysfunction induced by sevoflurane (SEV) anesthesia. Here, we examined the effects of LiCl on SEV‐induced cognitive dysfunction in rats and on SEV‐induced neuron apoptosis. We report that anesthesia with SEV significantly impaired memory performance, induced oxidative stress and hippocampal neuron apoptosis, and stimulated GSK‐3β activity. Treatment with LiCl ameliorated SEV‐induced cognitive disorder in rats by inhibiting the GSK‐3β/β‐catenin signaling pathway. In addition, LiCl reduced hippocampal neuron apoptosis and oxidative stress induced by SEV anesthesia. These results suggest that LiCl may have potential for development into a therapeutic agent for treatment of SEV anesthesia‐induced cognitive dysfunction.
机译:术后认知功能障碍是老年患者涉及麻醉后的老年患者的常见并发症,但潜在的机制明白很差。锂是双极性疾病的常规治疗,通过抑制脑和脊髓中的糖原合成酶激酶-3β(GSK-3β)施加各种疾病中的神经保护作用。然而,尚不清楚氯化锂(LICL)是否可以防止七氟醚(Sev)麻醉诱导的认知功能障碍。在这里,我们研究了LICL对大鼠的SEV诱导的认知功能障碍和SEV诱导的神经元细胞凋亡的影响。我们认为麻醉具有七,内存性能,诱导氧化应激和海马神经元细胞凋亡和刺激的GSK-3β活性。通过抑制GSK-3β/β-Catenin信号通路,LiCl治疗大鼠的ev诱导的认知疾病。此外,LiCL降低了Sev麻醉诱导的海马神经元细胞凋亡和氧化应激。这些结果表明,LiCL可能对治疗剂的潜力有潜力,用于治疗Zep麻醉诱导的认知功能障碍。

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