Peng Su, Xu Li, Ma Jin-Yu, Gu Xiao-Song, Sun Cheng
Key Laboratory for Neuroregeneration of Jiangsu Province and Ministry of Education, Co-Innovatioin Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China.
Neural Regen Res. 2018 Nov;13(11):1981-1987. doi: 10.4103/1673-5374.239446.
It has been well documented that Achyranthes bidentata polypeptides (ABPPs) are potent neuroprotective agents in several types of neurons. However, whether ABPPs protect dopaminergic neurons from apoptosis induced by neurotoxins is still unknown. This study was designed to observe the effect of ABPPk, a purified fraction of ABPPs, on apoptosis of dopaminergic neurons. SH-5YHY cells and primary dopaminergic neurons were pre-treated with ABPPk (25, 50, or 100 ng/mL) for 12 hours. Cells were then exposed to 6-hydroxydopamine (50 or 150 μM) or rotenone (50 or 200 μM) for 36 hours to induce cell apoptosis. Our results demonstrate that ABPPk markedly increased viability in SH-SY5Y cells and primary dopaminergic neurons, decreased lactate dehydrogenase activity and number of apoptotic dopaminergic neurons, elevated mitochondrial membrane potential, and increased Bcl-2/Bax ratio. These findings suggest that ABPPk protects dopaminergic neurons from apoptosis, and that ABPPk treatment might be an effective intervention for treating dopaminergic neuronal loss associated with disorders such as Parkinson's disease.
已有充分文献证明，牛膝多肽（ABPPs）在几种类型的神经元中是有效的神经保护剂。然而，ABPPs是否能保护多巴胺能神经元免受神经毒素诱导的凋亡仍不清楚。本研究旨在观察ABPPs的纯化组分ABPPk对多巴胺能神经元凋亡的影响。将SH-5YHY细胞和原代多巴胺能神经元用ABPPk（25、50或100 ng/mL）预处理12小时。然后将细胞暴露于6-羟基多巴胺（50或150 μM）或鱼藤酮（50或200 μM）36小时以诱导细胞凋亡。我们的结果表明，ABPPk显著提高了SH-SY5Y细胞和原代多巴胺能神经元的活力，降低了乳酸脱氢酶活性和凋亡多巴胺能神经元的数量，提高了线粒体膜电位，并增加了Bcl-2/Bax比值。这些发现表明，ABPPk可保护多巴胺能神经元免受凋亡，并且ABPPk治疗可能是治疗与帕金森病等疾病相关的多巴胺能神经元丢失的有效干预措施。
