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Lycium barbarum polysaccharides attenuates the apoptosis of hippocampal neurons induced by sevoflurane

机译:枸杞多糖减弱七氟醚诱导的海马神经元凋亡

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摘要

Following the application of inhalational anesthetics, including sevoflurane, patients may suffer from neural injury. The present study was conducted to explore the mechanism involved in Lycium barbarum polysaccharides (LBP) treatment of sevoflurane injured hippocampal neurons. Primary hippocampal neurons were isolated from Sprague Dawley embryonic rats. The Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Furthermore, flow cytometry (FCM) was used to determine cell proliferation and apoptosis rates. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were applied to detect the expression levels of apoptosis-related factors, including activated-Caspase-3, B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 associated X (Bax), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and total ERK1/2. The results showed that LBP promoted cell viability and cell proliferation but inhibited cell apoptosis in neurons injured with 3% sevoflurane, in dose-dependent manners (100, 200 and 400 µg/ml). LBP increased the expression levels of Bcl-2 and p-ERK1/2, and decreased levels of activated-Caspase-3 and Bax in a dose-dependent manner in hippocampal neurons that were injured with sevoflurane. In addition, ERK1/2 inhibitor reversed the above phenomenon in 400 µg/ml LBP and 3% sevoflurane-treated hippocampal neurons. Therefore, the present study indicated that LBP protected hippocampal neurons from sevoflurane injury, including aberrant cell apoptosis, via the ERK1/2 pathway.
机译:吸入麻醉药(包括七氟醚)后,患者可能会遭受神经损伤。进行本研究以探讨枸杞多糖(LBP)治疗七氟醚损伤的海马神经元的机制。从Sprague Dawley胚胎大鼠中分离出原代海马神经元。细胞计数试剂盒8(CCK-8)分析用于检测细胞活力。此外,流式细胞仪(FCM)用于确定细胞增殖和凋亡率。应用逆转录定量聚合酶链反应(RT-qPCR)和蛋白质印迹分析来检测凋亡相关因子的表达水平,包括活化的Caspase-3,B细胞淋巴瘤/白血病2(Bcl-2)和Bcl-2相关的X(Bax),磷酸化的细胞外信号调节激酶1/2(p-ERK1 / 2)和总ERK1 / 2。结果表明,LBP可以剂量依赖性(100、200和400 µg / ml)促进3%七氟醚损伤的神经元的细胞活力和细胞增殖,但抑制细胞凋亡。 LBP以剂量依赖性方式增加了七氟醚损伤的海马神经元中Bcl-2和p-ERK1 / 2的表达水平,并降低了活化的Caspase-3和Bax的水平。此外,ERK1 / 2抑制剂在400 µg / ml LBP和3%七氟醚处理的海马神经元中逆转了上述现象。因此,本研究表明,LBP通过ERK1 / 2途径保护海马神经元免受七氟醚损伤,包括异常细胞凋亡。

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