Ning Baile, Deng Minzhen, Zhang Qinxin, Wang Nanbu, Fang Yongqi
The Guangzhou University of Chinese Medicine, Guangzhou, China.
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, Guangzhou, 510405, China.
Neurochem Res. 2016 Aug;41(8):2097-101. doi: 10.1007/s11064-016-1922-0. Epub 2016 Apr 21.
Parkinson's disease (PD) is a neurodegenerative disease, with genetics and environment contributing to the disease onset. The limited pathological cognize of the disease restrained the approaches to improve the clinical treatment. Recently, studies showed that endoplasmic reticulum (ER) stress played an important role in the pathogenesis of PD. There was a neuroprotective effect partly mediated by modulating ER stress. β-Asarone is the essential constituent of Acorus tatarinowii Schott volatile oil. Our team observed that β-asarone could improve the behavior of parkinsonian rats; increase the HVA, Dopacl, and 5-HIAA levels; and reduce α-synuclein levels. Here we assumed that the protective role of β-asarone on parkinsonian rats was mediated via ER stress pathway. To prove the hypothesis we investigated the mRNA levels of glucose regulated protein 78 (GRP78) and C/EBP homologous binding protein (CHOP) in 6-hydroxy dopamine (6-OHDA) induced parkinsonian rats after β-asarone treatment. Furthermore, the inositol-requiring enzyme 1/X-Box Binding Protein 1 (IRE1/XBP1) ER stress pathway was also studied. The results showed that β-asarone inhibited the mRNA levels of GRP78 and CHOP, accompanied with the delined expressions of phosphorylated IER1 (p-IRE1) and XBP1. We deduced that β-asarone might have a protective effect on the 6-OHDA induced parkinsonian rats via IRE1/XBP1 Pathway. Collectively, all data indicated that β-asarone might be a potential candidate of medicine for clinical therapy of PD.
帕金森病（PD）是一种神经退行性疾病，其发病由遗传和环境因素共同作用。对该疾病有限的病理认知限制了改善临床治疗的方法。最近，研究表明内质网（ER）应激在PD的发病机制中起重要作用。通过调节ER应激可产生部分神经保护作用。β-细辛醚是石菖蒲挥发油的主要成分。我们的团队观察到β-细辛醚可以改善帕金森病大鼠的行为；提高高香草酸（HVA）、多巴胺（Dopacl）和5-羟色胺（5-HIAA）水平；并降低α-突触核蛋白水平。在此我们假设β-细辛醚对帕金森病大鼠的保护作用是通过ER应激途径介导的。为了验证这一假设，我们研究了β-细辛醚治疗后6-羟基多巴胺（6-OHDA）诱导的帕金森病大鼠中葡萄糖调节蛋白78（GRP78）和C/EBP同源结合蛋白（CHOP）的mRNA水平。此外，还研究了肌醇需求酶1/X盒结合蛋白1（IRE1/XBP1）ER应激途径。结果表明，β-细辛醚抑制了GRP78和CHOP的mRNA水平，同时伴随着磷酸化IRE1（p-IRE1）和XBP1表达的下降。我们推断β-细辛醚可能通过IRE1/XBP1途径对6-OHDA诱导的帕金森病大鼠具有保护作用。总体而言，所有数据表明β-细辛醚可能是PD临床治疗的潜在候选药物。
