目的:探究肉苁蓉总苷(GCs)对Aβ1-42寡聚体诱导小鼠海马神经元细胞系(HT22)细胞构建的阿尔茨海默病(AD)细胞模型突触可塑性的影响。方法:将HT22细胞分为对照组、模型组、空白大鼠血清组和GCs给药组。分别给予相应处理后记录各组细胞形态、活力以及突触相关mRNA和蛋白的表达水平情况。结果:与对照组相比,模型组细胞突触长度明显缩短、胞体较小、形态较差、凋亡细胞增多,细胞活力有所下降,脑源性神经营养因子(BDNF)、突触后致密蛋白(PSD-95)和N-甲基-D-天冬氨酸受体1(NMDAR1)的mRNA水平明显下降(P<0.05),PSD-95和NMDAR1的蛋白表达水平均显著下降(P<0.05);与模型组和空白大鼠血清组相比,GCs给药组的细胞突触长度、密度和细胞活力(P<0.05)均有所恢复,凋亡细胞的数量减少,BDNF、突触素(SYN)、PSD-95和NMDAR1的mRNA表达水平显著升高(P<0.05),NMDAR1和PSD-95蛋白的表达水平明显提高(P<0.05)。结论:GCs含药血清可明显提高AD细胞模型的突触可塑性,改善AD模型细胞病理进程。
郭鹏程
,
赵婧
,
张士滨
,
王储
,
徐晗
,
霍东升
,
闫旭升
,
杨占君
,
贾建新
. 肉苁蓉总苷对Aβ1-42寡聚体诱导的HT22细胞突触可塑性的影响*[J]. 包头医学院学报, 2024
, 40(9)
: 6
-12
.
DOI: 10.16833/j.cnki.jbmc.2024.09.002
Objective: To investigate the effect of general cistanosides (GCs) on synaptic plasticity of Alzheimer's disease (AD) cell model constructed by Aβ1-42 oligomer-induced mouse hippocampal neuron cell line (HT22) cells. Methods: HT22 cells were divided into control group, model group, blank rat serum group and GCs administration group. The morphology, viability and expression levels of synapse-related mRNA and proteins in each group were recorded. Results: Compared with the control group, the synaptic length of the model group was significantly shortened, the cell body was small, the morphology was poor, the apoptotic cells were increased, the cell viability was decreased, the mRNA levels of brain-derived neurotrophic factor (BDNF), postsynaptic density protein (PSD-95) and N-methyl-D-aspartate receptor 1 (NMDAR1) were significantly decreased (P<0.05), and the protein expression levels of PSD-95 and NMDAR1 were significantly decreased (P<0.05). Compared with the model group and the blank rat serum group, the synaptic length, density and cell viability(P<0.05) of the GCs administration group were restored, the number of apoptotic cells was decreased, the mRNA expression levels of BDNF, synaptophysin (SYN), PSD-95 and NMDAR1 were significantly increased (P<0.05), and the expression levels of NMDAR1 and PSD-95 proteins were significantly increased (P<0.05). Conclusion: Medicated serum of GCs can significantly improve the synaptic plasticity and pathological process of AD cell models.
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