Neuroprotective effect of formononetin against TBI in rats via suppressing inflammatory reaction in cortical neurons
Neuroprotective effect of formononetin against TBI in rats via suppressing inflammatory reaction in cortical neurons
复制标题
芒柄花素通过抑制皮质神经元炎症反应对大鼠 TBI 的神经保护作用
DOI：
10.1016/j.biopha.2018.06.041
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发表时间：
2018-10-01
影响因子：
7.5
通讯作者：
Zhang, Jianfeng
中科院分区：
文献类型：
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作者：
Li, Zhengzhao;Zeng, Guang;Zhang, Jianfeng
创伤性脑损伤（Traumatic brain injury，TBI）是指由外力引起的以大脑皮质坏死和细胞丢失为特征的脑损伤。有趣的是，一种名为芒柄花素（FN）的植物提取物被发现具有很好的药理活性，包括细胞神经保护。因此，我们认为FN可能对TBI产生生物保护作用，并讨论了其机制。在本研究中，通过Feeney的经典方法建立大鼠TBI模型，然后用不同浓度的FN治疗。Nissl-特殊和DAPI-标记的染色用于评估靠近损伤组织的皮质神经元的增殖。ELISA法测定血清和皮层神经元中白细胞介素6（IL 6）、肿瘤坏死因子α（TNF-α）和白细胞介素10（IL 10）的含量。采用免疫分析法和RT-PCR法检测脑内IL 10的表达水平。有趣的是，在FN处理的TBI大鼠模型中显示的结果表明皮质增殖升高。FN处理后，血清和皮质神经元中的IL 10水平升高，而血液中的TNF-α和IL 6水平降低。此外，FN处理的TBI大鼠模型中IL 10的mRNA和蛋白表达水平均以剂量依赖性方式上调。总的来说，我们目前的研究结果表明，FN提供了有效的神经保护对TBI，可能通过激活IL 10的表达在皮层神经元附近的病变组织抑制神经炎症反应。
Traumatic brain injury (TBI) refers to external force-induced brain damage, characterized with necrosis and cell loss in cerebral cortex. Interestingly, a plant-extract named formononetin (FN) is found to possess promising pharmacological activities, including cellular neuroprotection. Thus, we propose that FN may exert biological protection against TBI and discuss the underlying mechanism. In the current study, a rat TBI model was established via Feeney's classical method, followed by different concentrations of FN treatment. Nissl-special and DAPI-labeled stains were utilized to assess the proliferation of cortical neurons nearing lesioned tissue. The contents of interleukin-6 (IL6), tumor necrosis factor (TNF-alpha), and interleukin-10 (IL10) in serum and the cortical neurons were determined by ELISA. Further, intracephalic IL10 expression levels were detected through immunoassay and RT-PCR. Interestingly, the results exhibited within the FN-treated TBI rat model indicated elevated cortical proliferation. The levels of IL10 in serum and the cortical neurons were increased following FN treatments, while TNF-alpha and IL6 levels in the blood were decreased. In addition, both mRNA and protein expression levels of IL10 in the FN-treated TBI rat model were up-regulated in a dose-dependent manner. Collectively, our present findings indicate that FN provides effective neuroprotection against TBI, likely by activating IL10 expression in cortical neurons nearing lesioned tissue to inhibit neuroinflammatory reaction.