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首页> 外文期刊>Neurochemical research >Protective Role of Apocynin via Suppression of Neuronal Autophagy and TLR4/NF-κB Signaling Pathway in a Rat Model of Traumatic Brain Injury
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Protective Role of Apocynin via Suppression of Neuronal Autophagy and TLR4/NF-κB Signaling Pathway in a Rat Model of Traumatic Brain Injury

机译：在创伤性脑损伤大鼠模型中抑制神经元自噬和TLR4 / NF-κB信号传导途径的保护作用

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Abstract Neuronal autophagy and inflammatory responses are important in the pathogenesis of traumatic brain injury (TBI), and toll-like receptor 4 (TLR4) may play an important role in the related molecular cascade. The present study investigated the protective effect of apocynin, an inhibitor of NADPH oxidase, in a TBI rat model and further examined neuronal autophagy and the TLR4-mediated pathway. Adult male Sprague-Dawley rats were subjected to controlled cortical impact injury and intraperitoneally injected with apocynin (50?mg/kg) immediately after the trauma. In addition to motor and behavioral studies, brain water content and histology analyses were performed. Expression of autophagy-related proteins as well as TLR4/NF-κB signaling and inflammatory mediators was analyzed. The apocynin treatment significantly attenuated TBI-induced motor and behavioral impairment, brain edema and neuronal damage in rats. Immunohistochemical and Western blot analyses revealed that apocynin treatment significantly reduced the expression of NOX 2 , LC3 and Beclin1 in the hippocampus at 12–48?h after injury. Double immunolabeling demonstrated that apocynin decreased the co-localization of LC3 or TLR4-positive cells with hippocampal neurons at 24?h following TBI. In addition, CD11b (microglial marker) and GFAP (astrocyte marker)-immunopositive cells were also clearly decreased in hippocampal tissues. Meanwhile, protein levels of TLR4, NF-κB p65, TNF-α and IL-1β were found to be significantly downregulated by Western blot analysis. In conclusion, our findings indicate that the protective effects of apocynin may be related to modulation of neuronal autophagy and the TLR4/NF-κB signaling pathway.
机译：摘要神经元自噬和炎症反应在创伤性脑损伤（TBI）的发病机制中是重要的，并且Toll样受体4（TLR4）可能在相关的分子级联中起重要作用。本研究研究了呼吸皂苷蛋白，NADPH氧化酶的抑制剂，在TBI大鼠模型中的保护作用，进一步检查神经元自噬和TLR4介导的途径。将成年雄性Sprague-Dawley大鼠进行受控皮质冲击损伤，并在创伤后立即用呼吸昔肽（50×mg / kg）腹膜内注射。除电机和行为研究外，还进行脑含水量和组织学分析。分析了与自噬相关蛋白以及TLR4 / NF-κB信号传导和炎症介质的表达。呼吸植检素治疗明显减弱了TBI诱导的电动机和行为损伤，脑水肿和大鼠神经元损伤。免疫组织化学和Western印迹分析显示，肺炎素治疗显着降低了损伤后12-48ΩHIPPocampus中NOx 2，LC3和BECLIN1的表达。双免疫标签表明，呼吸植入蛋白在TBI之后在24μmHippodampal神经元中降低了LC3或TLR4阳性细胞的共定位。此外，在海马组织中也显然降低了CD11b（微胶质标记物）和GFAP（星形胶质细胞标志物） - 免疫阳性细胞。同时，发现通过Western印迹分析显着下调TLR4，NF-κBP65，TNF-α和IL-1β的TLR4，NF-κBP65，TNF-α和IL-1β的蛋白质水平。总之，我们的研究结果表明，呼吸植入素的保护作用可能与神经性自噬和TLR4 / NF-κB信号传导途径的调节有关。

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