Department of Life Science, Biomedi Campus, Dongguk University-Seoul, 32 Dongguk-ro, Ilsandong-gu, Goyang-si 10326, Gyeonggi-do, Korea.
Int J Mol Sci. 2020 Dec 2;21(23):9202. doi: 10.3390/ijms21239202.
has diverse biological activities, such as antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. This study investigated the protective effects of fruit extracts (CTFE) against scopolamine (SCO)-induced neuron impairment. The neuroprotective effects of CTFE on SCO-induced memory dysfunction were confirmed in mice using the Barnes maze test. The results showed that co-treatment of SCO and CTFE increased the stay time in the target zone compared with SCO treatment alone. Similarly, the results obtained by the fear conditioning test revealed that SCO-CTFE co-treatment induced the freezing action time under both the contextual fear condition and the cued fear condition compared with SCO treatment alone. Moreover, we showed that CTFE reduced the SCO-induced acetylcholinesterase (AChE) activity, thereby increasing the acetylcholine concentration in mice hippocampal tissues. Consistent with the improvement of memory and recognition function in vivo, our in vitro results showed that CTFE induced cAMP response element binding protein (CREB) and extracellular regulated kinase 1/2 (ERK1/2) activity in PC12 cells and reduced SCO-induced AChE activity. In addition, the microarray results of the hippocampal tissue support our data showing that CTFE affects gene expressions associated with neurogenesis and neuronal cell differentiation markers such as and . Overall, CTFE exerts a neuroprotective effect via regulation of the CREB and ERK1/2 signaling pathways and could be a therapeutic candidate for neurodegenerative diseases.
具有多种生物活性,如抗氧化、抗炎、抗癌和神经保护作用。本研究探讨了 果提取物 (CTFE) 对东莨菪碱 (SCO) 诱导的神经元损伤的保护作用。通过巴恩斯迷宫试验证实 CTFE 对 SCO 诱导的记忆功能障碍具有保护作用。结果表明,与 SCO 单独处理相比,SCO 和 CTFE 共同处理增加了目标区域的停留时间。同样,恐惧条件试验的结果表明,与 SCO 处理相比,SCO-CTFE 共同处理诱导了上下文恐惧条件和提示恐惧条件下的冻结作用时间。此外,我们表明 CTFE 降低了 SCO 诱导的乙酰胆碱酯酶 (AChE) 活性,从而增加了小鼠海马组织中的乙酰胆碱浓度。与体内记忆和识别功能的改善一致,我们的体外结果表明 CTFE 诱导 PC12 细胞中的 cAMP 反应元件结合蛋白 (CREB) 和细胞外调节激酶 1/2 (ERK1/2) 活性,并降低了 SCO 诱导的 AChE 活性。此外,海马组织的基因芯片结果支持我们的数据表明,CTFE 影响与神经发生和神经元细胞分化标志物相关的基因表达,如 和. 总之,CTFE 通过调节 CREB 和 ERK1/2 信号通路发挥神经保护作用,可能是神经退行性疾病的治疗候选药物。