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Asphyxial hypoxic preconditioning induces neuroprotective effect via activation of toll-like receptor 4 (TLR4) signal pathway in rats

机译:窒息缺氧预处理通过激活Toll样受体4(TLR4)信号通路诱导神经保护作用

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Hypoxic preconditioning (HP) induces neuroprotective effect against cerebral ischemia, but the mechanism still remains unclear. In this study, we investigated whether the toll-like receptor 4 (TLR4) signal pathway was involved in cerebral ischemic tolerance. According to the treatment of HP and asphyxial cardiac arrest (ACA), rats were assigned to ACA group, HP + ACA group, HP group and Sham group. Rat mortality was 5% in HP + ACA group and 30% in ACA group (P&0.01); neurofunctional scores in HP and HP + ACA group were better than in ACA group (P&0.05). Compared with Sham group, TLR4 mRNA expression, NF-кB activity and the production of TNF-α and IL-6 in HP or HP + ACA or ACA group were significantly increased. The increase was progressively significant in groups (AHP & AHP + ACA & ACA) (P&0.01). HP induced mild inflammation via activating the TLR4 signal pathway and then further inhibited inflammatory response induced by ACA.
机译:缺氧预处理(HP)可以诱导针对脑缺血的神经保护作用,但其机制仍不清楚。在这项研究中,我们调查了Toll样受体4(TLR4)信号通路是否参与脑缺血耐受。根据HP和窒息性心脏骤停(ACA)的治疗,将大鼠分为ACA组,HP + ACA组,HP组和假手术组。 HP + ACA组的大鼠死亡率为5%,ACA组的大鼠死亡率为30%(P <0.01)。 HP和HP + ACA组的神经功能评分优于ACA组(P <0.05)。与假手术组相比,TLR4 mRNA表达,NF-κB活性和TNF-α的产生均高于正常对照组。 HP或HP + ACA或ACA组的IL-6和IL-6均明显升高。各组的增加是逐步显着的(AHP <AHP + ACA <ACA)(P <0.01)。 HP通过激活TLR4信号途径诱导轻度炎症,然后进一步抑制ACA诱导的炎症反应。

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