Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway.

IF 2.2 4区医学 Q2 MEDICINE, GENERAL & INTERNAL Clinics Pub Date : 2024-12-20 eCollection Date: 2024-01-01 DOI:10.1016/j.clinsp.2024.100560

Lijuan Lin, Chenhui Zhu, Bing Yan, Pinxian Yu, Liu Yang, Wei Huang, Junren Chen

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Abstract

Background: Sevoflurane (Sev) is an inhalational anesthetic for surgical procedures where it can trigger cognitive dysfunction and neuronal apoptosis. Gyosaponin (GpS) was studied for its effects on brain morphology and cognitive behaviors in Sev-anesthetized rats.

Methods: Male Sprague-Dawley rats were induced by 3 % Sev anesthesia, and 25 mg/kg and 100 mg/kg GpS were injected into the rats by tail vein. The in vitro model of Sev anesthesia was constructed by treating primary rat hippocampal neurons with 4.1 % Sev in the presence of GpS (5, 10, and 20 μM). The neuroprotective effects of GpS against Sev-induced cognitive deficits in rats were evaluated using the open field and Morris water maze tests. The apoptosis of hippocampal neurons was observed using HE staining and TUNEL assay. Apoptosis-related proteins and proteins related to the PI3K/Akt/mTOR pathway were determined via Western blot. Also, pro-inflammatory factors were measured via ELISA.

Results: GpS diminished the Sev-triggered apoptosis in neurons and Cleaved caspase-3, BAX, TNF-α, IL-6, lessened oxidative stress damage, and stimulated the PI3K/Akt/mTOR pathway. GpS therapy markedly enhanced learning and memory abilities in rats suffering from Sev-related cognitive impairments.

Conclusion: GpS ameliorates Sev-induced neurotoxicity and cognitive dysfunction by modulating the PI3K/Akt/mTOR pathway and alleviating neuronal apoptosis and oxidative stress.

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焦糖皂苷通过调节PI3K/AKT/mTOR通路改善七氟醚麻醉诱导的大鼠认知功能障碍和神经元凋亡。

背景：七氟醚（Sev）是一种用于外科手术的吸入麻醉剂，可引发认知功能障碍和神经元凋亡。研究了焦糖皂苷（GpS）对七次麻醉大鼠脑形态和认知行为的影响。方法：雄性Sprague-Dawley大鼠经3%七维麻醉诱导，经尾静脉注射25 mg/kg和100 mg/kg的GpS。在5、10、20 μM的GpS作用下，以4.1%的Sev处理原代大鼠海马神经元，建立Sev麻醉体外模型。采用开阔场和Morris水迷宫实验，评价gp对sev诱导的大鼠认知缺陷的神经保护作用。采用HE染色和TUNEL法观察海马神经元凋亡情况。Western blot检测凋亡相关蛋白和PI3K/Akt/mTOR通路相关蛋白。ELISA法检测促炎因子。结果：GpS可减少sev触发的神经元凋亡，并可裂解caspase-3、BAX、TNF-α、IL-6，减轻氧化应激损伤，刺激PI3K/Akt/mTOR通路。全科医生治疗显著提高了sev相关认知障碍大鼠的学习和记忆能力。结论：GpS通过调节PI3K/Akt/mTOR通路，减轻神经元凋亡和氧化应激，改善sev诱导的神经毒性和认知功能障碍。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinics 医学-医学：内科

CiteScore

4.10

自引率

3.70%

发文量

129

审稿时长

52 days

期刊介绍： CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.