We evaluated the effectiveness of Scrophularia buergeriana extract (Brainon) on cognitive dysfunction and determined its underlying mechanisms in a scopolamine (SCO)-treated mouse model of memory impairment. Brainon treatment for 28 days ameliorated the symptoms of memory impairment as indicated by the results of both passive avoidance performance and the Morris water mazes. Brainon lowered acetylcholinesterase activity and raised acetylcholine levels in the hippocampus. The treatment elevated the protein levels of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element-binding (CREB). Additionally, the excessive generation of SCO-induced reactive oxygen species (ROS) and subsequent oxidative stress were suppressed by the enhancement of superoxide dismutase (SOD)-1 and SOD-2 proteins. mRNA levels of upregulated interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, as well as the apoptotic protein Bcl-2-associated X protein (Bax), cleaved caspase-9, and cleaved poly adenosine diphosphate-ribose polymerase (PARP) expression after SCO injection were downregulated by Brainon treatment. Collectively, these findings suggested that Brainon possesses anti-amnesic effects through the CREB-BDNF pathway. Moreover, it exerted antioxidant, anti-inflammatory, and anti-apoptotic effects in SCO-induced mice exhibiting cognitive impairment and memory loss.

中文翻译：

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玄参提取物（Brainon）通过CREB-BDNF信号通路改善东S碱诱导的小鼠神经元损伤和胆碱能功能障碍。

我们评估了玄参的功效提取物（大脑）对认知功能障碍的影响，并在东pol碱（SCO）处理的记忆障碍小鼠模型中确定了其潜在机制。被动回避表现和Morris水迷宫的结果表明，Brainon治疗28天可减轻记忆障碍的症状。Brainon降低了海马体中的乙酰胆碱酯酶活性并提高了乙酰胆碱水平。该治疗提高了脑源性神经营养因子（BDNF）和磷酸化的cAMP反应元件结合（CREB）的蛋白质水平。此外，通过增加超氧化物歧化酶（SOD）-1和SOD-2蛋白，可以抑制SCO诱导的活性氧（ROS）的过量生成和随后的氧化应激。上调白介素（IL）-1β，IL-6和肿瘤坏死因子（TNF）-α的mRNA水平，以及通过Brainon处理​​下调了SCO注射后凋亡蛋白Bcl-2相关X蛋白（Bax），裂解的caspase-9和裂解的聚腺苷二磷酸核糖聚合酶（PARP）的表达。总体而言，这些发现表明Brainon通过CREB-BDNF途径具有抗记忆删除作用。此外，它在SCO诱导的小鼠中表现出抗氧化，抗炎和抗凋亡的作用，这些小鼠表现出认知障碍和记忆力减退。