芥子酸对Aβ1-42致PC12细胞损伤的改善作用及对BDNF/TrkB/ERK信号通路的影响-中国药房

芥子酸对Aβ1-42致PC12细胞损伤的改善作用及对BDNF/TrkB/ERK信号通路的影响

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篇名：	芥子酸对Aβ1-42致PC12细胞损伤的改善作用及对BDNF/TrkB/ERK信号通路的影响
TITLE：	Effects of Sinapic Acid on Improving PC 12 Cell Damage Induced by Aβ1-42 and BDNF/TrkB/ERK Signaling Pathway
摘要：	目的：研究芥子酸对β-淀粉样蛋白1-42（Aβ1-42）诱导的大鼠肾上腺髓质嗜铬细胞瘤细胞（PC12细胞）损伤的改善作用，并探讨其对脑源性神经营养因子（BDNF）/酪氨酸激酶B（TrkB）/细胞外信号调节激酶（ERK）信号通路的影响。方法：将PC12细胞分为空白组、模型组和芥子酸低、高剂量组（50、100μmol/L）。除空白组外，其余各组均用2μmol/L的Aβ1-42诱导细胞损伤；建模24h后，药物组加入相应药液，培养24h。观察各组细胞形态变化，检测细胞存活率和细胞中BDNFmRNA的表达情况及其蛋白水平，以及TrkB、ERK1/2、磷酸化ERK1/2（p-ERK1/2）蛋白的表达情况，并计算p-ERK1/2与ERK1/2的比值（p-ERK/ERK比值）。结果：与空白组比较，模型组细胞突触变短，细胞连接较松，贴壁性差，胞质较暗淡，胞浆中有较多颗粒，细胞存活率以及细胞中BDNFmRNA的相对表达量及其蛋白水平，TrkB、p-ERK1/2蛋白的相对表达量和p-ERK/ERK比值均显著降低（P＜0.05或P＜0.01）。与模型组比较，芥子酸高剂量组细胞病理变化明显改善，细胞存活率以及细胞中BDNFmRNA的相对表达量及其蛋白水平，TrkB、p-ERK蛋白的相对表达量和p-ERK/ERK比值均显著升高（P＜0.05或P＜0.01）。结论：芥子酸可改善Aβ1-42诱导的PC12细胞损伤，其作用机制可能与激活BDNF/TrkB/ERK信号通路有关。
ABSTRACT：	OBJECTIVE：To study the improvement effects of sinapic acid （SA）on PC 12 cell damage induced by Aβ1-42，and to investigate its effect on brain-derived neurotrophic factor （BDNF）/tyrosine kinase B （TrkB）/extracellular signal-regulated kinase （ERK）signaling pathway. METHODS ：PC12 cells were divided into blank group ，model group ，SA low-dose and high-dose groups（50，100 μmol/L）. Except for blank group ，cell damage was induced by Aβ1-42 in other groups ；24 h after modeling ， administration groups were added with the corresponding solution and cultured for 24 h. Morphological changes of cells in each group were observed. Cell survival rate ，mRNA expression and protein level of BDNF ，protein expression of TrkB ，ERK1/2 and phosphorylated ERK 1/2（p-ERK1/2）were detected. p-ERK/ERK ratio was calculated. RESULTS ：Compared with blank group ，the model group had shorter synapses ，looser intercellular junctions ，poor adhesion ，dim cytoplasm and more granules in cytoplasm. Cell survival rate and mRNA expression and protein level of BDNF ，the relative expression of TrkB and p-ERK 1/2 protein，p-ERK/ ERK ratio were significantly decreased （P＜0.05 or P＜0.01）. Compared with model group ，in SA high-dose group the pathological changes of the cells were significantly improved ，the survival rate of the cells ，the mRNA expression and protein level of BDNF，the relative expression of TrkB and p-ERK 1/2 protein， p-ERK/ERK ratio were significantly increased （P＜0.05 or P＜ 0.01）. CONCLUSIONS：SA can i mprove PC 12 cells damage induced by Aβ1-42，the mechanism of which may be associated with activating BDNF/TrkB/ERK signaling pathway. qq.com
期刊：	2021年第32卷第10期
作者：	薛迪，刘宇超，汪娜，刘学伟
AUTHORS：	XUE Di，LIU Yuchao ，WANG Na，LIU Xuewei
关键字：	芥子酸；阿尔茨海默症；β-淀粉样蛋白1-42；脑源性神经生长因子；酪氨酸激酶B；细胞外信号调节激酶
KEYWORDS：	Sinapic acid ；Alzheimer’s disease ；A β 1-42；
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