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首页> 外文期刊>Molecular medicine reports >Role of the Toll-like receptor 3 signaling pathway in the neuroprotective effect of sevoflurane pre-conditioning during cardiopulmonary bypass in rats
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Role of the Toll-like receptor 3 signaling pathway in the neuroprotective effect of sevoflurane pre-conditioning during cardiopulmonary bypass in rats

机译：Toll样受体3信号通路在大鼠体外循环期间七氟醚预处理的神经保护作用中的作用

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摘要

The aim of the present study was to explore the roles and possible molecular mechanism of the alleviating effect of sevoflurane pre-treatment on the extracorporeal circulation and to investigate the possible involvement of the Toll-like receptor (TLR3) signaling pathway. A total of 64 male Sprague Dawley rats were randomly divided into three groups: The sham operation group (H group; n=8), cardiopulmonary bypass (CPB) group (C group; n=24) and sevoflurane pre-conditioning group (S group; n=32). The C group was subjected to tracheal intubation and mechanical ventilation, vessel puncture and catheter placement in the right femoral artery and right internal jugular vein, while no CPB was performed in the H group. The S group was pre-treated with 2.4% sevoflurane for 1 h prior to establishing the CPB model. The CPB in the C and S groups was performed for 1 h. Blood of the rats was analyzed and clinical parameters were detected prior to, during and at various time-points after CPB. In addition, eight rats from the C and S groups each were sacrificed at these time-points and brain tissue samples were analyzed. The levels of the brain damage-specific protein S100- as well as IL-6 and IFN- in the serum were detected by ELISA; furthermore, the expression levels of TLR3 and TIR-domain-containing adapter-inducing interferon- (TRIF) in the left hippocampus were assessed by ELISA and/or western blot analysis. The right hippocampus was assessed for neuronal apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The mean arterial pressure, heart rate and hematocrit were significantly decreased following CPB (P<0.05), while there was no significant changes in any other clinical parameters. The serum levels of S100- and IL-6 in the C group were significantly increased compared with those in the H group (P<0.05), which was attenuated by sevoflurane-pre-treatment. Compared with the H group, the serum levels of IFN- as well as hippocampal protein levels of TLR3 and TRIF were significantly increased in the C group during and after CPB (P<0.05), which was markedly aggravated in the S group (P<0.05). The number of apoptotic hippocampal neurons, although being generally low, was significantly increased in the C group compared with that in the H group (P<0.05), while apoptosis was significantly attenuated by sevoflurane-pre-treatment (P<0.05). The present study therefore concluded that 2.4% sevoflurane pre-treatment has a protective effect on the rat brain against CPB-induced injury, which may be mediated via the TLR3 signaling pathway through upregulating the expression levels of anti-inflammatory and downregulating pro-inflammatory proteins.
机译：本研究的目的是探讨七氟醚预处理对体外循环的缓解作用和可能的分子机制，并探讨Toll样受体（TLR3）信号传导途径的可能参与。总共将64只雄性Sprague Dawley大鼠随机分为三组：假手术组（H组; n = 8）;体外循环（CPB）组（C组; n = 24）和七氟醚预处理组（S）组; n = 32）。 C组在右股动脉和右颈内静脉进行气管插管和机械通气，穿刺和导管置入，而H组则未进行CPB。在建立CPB模型之前，S组用2.4％的七氟醚预处理1小时。 C组和S组的CPB进行1小时。在CPB之前，期间和之后的各个时间点分析大鼠的血液并检测临床参数。另外，在这些时间点处死了来自C和S组的八只大鼠，并分析了脑组织样品。 ELISA法检测血清中脑损伤特异性蛋白S100-以及IL-6和IFN-的水平。此外，通过ELISA和/或蛋白质印迹分析评估了左海马中TLR3和含TIR结构域的衔接子-诱导干扰素（TRIF）的表达水平。通过末端脱氧核苷酸转移酶dUTP缺口末端标记测定法评估右海马的神经元凋亡。 CPB后平均动脉压，心率和血细胞比容显着降低（P <0.05），而其他任何临床参数均无显着变化。 C组患者血清S100和IL-6水平较H组明显升高（P <0.05），七氟醚预处理可降低血清S100和IL-6水平。与H组相比，C组在CPB期间和之后血清IFN-水平以及TLR3和TRIF的海马蛋白水平显着升高（P <0.05），而S组则明显加重（P <0.05）。 0.05）。 C组的凋亡海马神经元数量虽然通常较低，但与H组相比却显着增加（P <0.05），而七氟醚预处理则显着减弱了细胞凋亡（P <0.05）。因此，本研究得出的结论是2.4％的七氟醚预处理对大鼠脑具有保护作用，可防止CPB诱导的损伤，这可能是通过TLR3信号通路通过上调抗炎蛋白的表达水平和下调促炎蛋白来介导的。 。

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