It is unclear whether β-asarone has a good antidepressant effect and what is the main mechanism in Depression in Parkinson’s disease (DPD) model rats. In this study, DPD model rats were screened from 6-OHDA induced rats by sucrose preference test (SPT) and forced swimming test (FST). DPD model rats were divided into eight groups: model group, pramipexole group, β-asarone low-dose group (β-asarone 7.5 group), β-asarone medium-dose group (β-asarone 15 group), β-asarone high-dose group (β-asarone 30 group), 3-MA group, rapamycin group, and PI3K inhibitor group. 28 days after the end of treatment, open field test (OFT), SPT and FST were conducted in rats. The level of α-synuclein (α-syn) in the striatum was determined by enzyme-linked immunosorbent assay (ELISA). The expression of Beclin-1, p62 in the striatum was determined by western blot. The expression of PI3K, p-PI3K, Akt, p-Akt, mTOR, p-mTOR, Beclin-1, and p62 in the hippocampus was determined by western blot. The spine density of neurons in the hippocampus was detected by golgi staining. The results showed that 4-week oral administration of β-asarone improve the motor and depressive symptoms of DPD model rats, and decrease the content of α-syn in the striatum. β-asarone inhibited the expression of autophagy in the striatum of DPD model rats. Furthermore, β-asarone decreased the levels of Beclin-1 protein, increased the expression of p62, p-PI3K, p-AKT, and p-mTOR, and improved the density of neuron dendritic spine in the hippocampus. We concluded that β-asarone might improve the behavior of DPD model rats by activating the PI3K/Akt/mTOR pathway, inhibiting autophagy and protecting neuron.

中文翻译：

---

β-细辛脑通过激活帕金森病抑郁大鼠模型中的 PI3K/Akt/mTOR 通路抑制自噬

β-细辛脑是否具有良好的抗抑郁作用以及帕金森病（DPD）模型大鼠抑郁的主要机制尚不清楚。本研究通过蔗糖偏好试验(SPT)和强迫游泳试验(FST)从6-OHDA诱导的大鼠中筛选DPD模型大鼠。 DPD模型大鼠分为8组:模型组、普拉克索组、β-细辛脑低剂量组(β-细辛脑7.5组)、β-细辛脑中剂量组(β-细辛脑15组)、β-细辛脑高剂量组。剂量组（β-细辛脑30组）、3-MA组、雷帕霉素组、PI3K抑制剂组。治疗结束后28天，对大鼠进行旷场试验（OFT）、SPT和FST。通过酶联免疫吸附测定（ELISA）测定纹状体中α-突触核蛋白（α-syn）的水平。 Western blot检测纹状体中Beclin-1、p62的表达。通过蛋白质印迹法测定海马中 PI3K、p-PI3K、Akt、p-Akt、mTOR、p-mTOR、Beclin-1 和 p62 的表达。高尔基染色检测海马神经元棘密度。结果显示，口服β-细辛脑4周可改善DPD模型大鼠的运动和抑郁症状，并降低纹状体中α-syn的含量。 β-细辛脑抑制DPD模型大鼠纹状体自噬的表达。此外，β-细辛醚降低了 Beclin-1 蛋白的水平，增加了 p62、p-PI3K、p-AKT 和 p-mTOR 的表达，并提高了海马神经元树突棘的密度。我们认为β-细辛脑可能通过激活PI3K/Akt/mTOR通路、抑制自噬、保护神经元来改善DPD模型大鼠的行为。