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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. [ABSTRACT FROM AUTHOR]

The primary aim of this study was to examine the correlation between the formation of Aβ plaques and autophagy, which is regulated by β-asarone and the lncRNA BACE1-AS. Additionally, the study sought to explore potential targets of the drug in inhibiting the deposition of toxic AD-related proteins and restoring impaired mitochondrial and autophagic functions. SHY5Y cells were utilized to construct a stable Alzheimer's disease (AD) model, followed by the utilization of interference and overexpression lentiviruses targeting BACE1-AS to establish a cell model. The cells were categorized into five groups, including a normal group, siRNA/BACE1 group, and β-asarone group. The fluorescence quantitative PCR technique was employed to assess the disparity in BACE1 mRNA expression, while changes in immunofluorescence (IF) were observed to determine the stable interference titre and action time of the lentiviruses. Additionally, western blotting (WB) and fluorescence quantitative PCR were employed to evaluate the expression of proteins and mRNAs associated with AD and autophagy. The findings demonstrated a significant elevation in BACE1 expression levels in brain tissue among individuals with AD compared to those without the condition. Moreover, the results indicated that the introduction of β-asarone led to an increase in the expression of the BACE1-AS gene in the cell group transfected with plasmid H12732. Furthermore, it was observed that β-asarone enhanced the expression levels of shRNA and BACE1 after 72 h. In contrast, β-asarone suppressed the expression of PS1, Aβ, BACE1, APP, and p62, while promoting the expression of syn, LC3 I/II, and Beclin-1. Based on these findings, it can be concluded that β-Asarone exerts a comprehensive influence on the expression of proteins associated with AD and synaptic function. β-Asarone exhibits the potential to mitigate Aβ deposition by impeding the expression of lncBACE1, thereby facilitating autophagy through the suppression of BACE1's inhibitory impact on autophagy. This complements the self-enhancing effect of autophagy. [ABSTRACT FROM AUTHOR]

Acupuncture has demonstrated its efficacy as a treatment for Parkinson's disease (PD). Thus, the objective of this study was to investigate the potential mechanisms underlying acupuncture's effects on PD treatment. Our approach involved several steps. Firstly, we assessed the behavioral changes in PD rats, the modulation of dopamine (DA) and 5-hydroxytryptamine (5-HT) levels in the striatum, as well as the alteration in α-synuclein (α-syn) levels in the midbrain, aiming to evaluate the efficacy of acupuncture in PD treatment. Secondly, we selected endoplasmic reticulum (ER) stress inhibitors and activators to assess the impact of ER stress on PD rats. Lastly, we utilized an IRE1 inhibitor to observe the influence of acupuncture on the IRE1/XBP1 pathway in PD rats. The findings of this study revealed that acupuncture improved the autonomous motor function, balance ability, coordination, and sensory motor integration function in the PD model rats. Additionally, it increased the levels of DA and 5-HT in the striatum while decreasing the levels of α-syn in the midbrain. Acupuncture also activated the expression of ER stress in the midbrain and upregulated the expression of IRE1/XBP1 in the striatum of PD model rats. Based on these results, we concluded that acupuncture may enhance the behavior of PD rats by activating the IRE1/XBP1 ER stress pathway, associated with the reduction of midbrain α-syn expression and the increase in striatal DA and 5-HT levels in unilateral 6-OHDA lesioned rats. [Display omitted] [ABSTRACT FROM AUTHOR]