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Background β‐asarone (β‐as), a compound extracted from Acorus calamus, has been found to have anticancer effects on a variety of human cancers. However, the potential effect of β‐as on bladder cancer (BCa) remains unknown. Methods After exposure to β‐as, migration, invasion, and epithelial‐mesenchymal transition (EMT) of BCa were determined by wound healing, transwell, and Western blot assays. Expression of proteins involved in the EMT and ER stress were explored by Western blot assays. Nude mouse xenograft model was served as the model system in vivo. Results The migration, invasion, and EMT of BCa were significantly inhibited after β‐as treatment. Further experiments revealed that endoplasmic reticulum (ER) stress is involved in β‐as‐mediated metastasis inhibition. In addition, β‐as significantly up‐regulated activating transcription factor 6 (ATF6), a branch of ER stress, and promoted its Golgi cleavage and nuclear localization. ATF6 silencing attenuated β‐as‐mediated metastasis and EMT inhibition in BCa cells. Conclusion Our data suggests that β‐as inhibits migration, invasion, and EMT of BCa by activating the ATF6 branch of ER stress. Thus, β‐as represents a potential candidate for BCa treatment. Schematic diagram illustrating the effects of β‐as in BCa based on the data obtained from this study: β‐as inhibits the migration, invasion and EMT of BCa cells by activating ER stress.

Accumulation of β-amyloid (Aβ) causes oxidative stress, which is the major pathological mechanism in Alzheimer’s disease (AD). β-asarone could reduce Aβ-induced oxidative stress and neuronal damage, but the molecular mechanism remains elusive. In this study, we used an Aβ-stimulated PC12 cell model to explore the neuroprotective effects and potential mechanisms of β-asarone. The results showed that β-asarone could improve cell viability and weaken cell damage and apoptosis. β-asarone could also decrease the level of ROS and MDA; increase the level of SOD, CAT, and GSH-PX; and ameliorate the mitochondrial membrane potential. Furthermore, β-asarone could promote the expression of Nrf2 and HO-1 by upregulating the level of PI3K/Akt phosphorylation. In conclusion, β-asarone could exert neuroprotective effects by modulating the P13K/Akt/Nrf2 signaling pathway. β-asarone might be a promising therapy for AD.

β-Asarone is a major component of Schott. It has pharmacological effects that include antihyperlipidemic, anti-inflammatory, and antioxidant activity. In the present study, the effect of β-asarone on neurodegeneration induced by intrahippocampal administration of β-amyloid was investigated in adult male Wistar rats. The rats were randomly divided into 9 groups: normal control, sham-operated control, β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) alone, Alzheimeric control rats (β-amyloid, intrahippocampal), β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) together with β-amyloid, and treatment was performed accordingly. Animals were injected with β-amyloid bilaterally. Animals received β-asarone daily using an intragastric tube for 50 days, starting from 30 days before administration of the β-amyloid. The rats were sacrificed and parameters of oxidative stress, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activity were measured in hippocampus homogenate. Histopathological changes were examined by Bielschowsky staining. Our results showed that administration of β-asarone (25 and 50 mg/kg) significantly increased the levels of antioxidant enzymes, including SOD (1.09 ±0.02, 1.21 ±0.02, < 0.001, respectively) and GPX (58.94 ±0.78, 68.92 ±3.64, < 0.001, respectively) in comparison with Alzheimeric control rats (SOD and GPX level for Alzheimeric control group: 0.44 ±0.01, 35.09 ±1.15, respectively). Histopathological examination showed that β-asarone decreased cell loss in the cerebral cortex and hippocampus in Alzheimeric rats. These results indicate that β-asarone is effective in providing protection against oxidative stress and neuronal damage induced by β-amyloid.

Alzheimer's disease (AD) is one of the most common types of dementia that causes memory, thinking, and behavior problems. The most important feature of AD is the gradual irreversible loss of cognitive ability through the formation of amyloid β (Aβ) plaques and neurofibrillary tangles composed of tau protein. The metabolism of Aβ and tau proteins is closely related to and is affected by autophagy. Current research speculates that autophagy dysfunction leads to an increase in harmful proteins in AD. β-Asarone is the main constituent of Schott and has important effects on the central nervous system. In this paper, we primarily explored the effects of β-asarone on the clearance of noxious proteins and the associated potential mechanisms autophagy in a PC12 cell AD model. A CCK-8 assay and LDH experiments were used to assess cell viability/toxicity, and SPiDER-βGal was used to detect cellular senescence. The important proteins associated with the pathogenesis of AD including APP, PS1, Aβ, BACE1, and SYN1 were analyzed by immunofluorescence (IF) and Western blot analysis. Antimycin A (A3) and cyclosporine A (CSA) were selected as the activators and inhibitors of autophagy, respectively. LC3, BECN, P62, PINK1, and Parkin protein expression were also examined by IF and Western blot analysis. The data showed that β-asarone administration significantly dose-dependently increased cell proliferation and decreased cytotoxicity; moreover, β-asarone inhibited SA-βGal and improved cell senescence. The results further showed that, compared to the model, APP, PS1, Aβ, BACE1, and p62 were reduced, while SYN1, BECN1, and LC3 were increased after treatment with β-asarone. The results of Canonical Correlation Analysis (CCA) showed a highly significant relationship between the pathological factors of AD and the protein expression of autophagy. In conclusion, our study demonstrated that β-asarone can inhibit Aβ, and this effect may occur by promoting autophagy in a cell model of AD.

Bemisia tabaci is a threat to agriculture worldwide because of its potential to cause devastating damage to various crops. β-asarone is a bioactive pesticidal chemical originating from Acorus calamus (or “Sweet Flag”) plants, and it displays significant lethal effects against insect pests. In this study, we established a baseline of susceptibility to β-asarone from China and patterns of cross-resistance to other popular insecticides. We found that all the 12 field-collected B. tabaci populations exhibited high susceptibility to β-asarone, and there was no cross-resistance detected for other tested insecticides. We subsequently evaluated the sublethal effects of β-asarone on physiology and biochemistry via LC25 treatment (4.7 mg/L). LC25 of β-asarone resulted in prolonged developmental duration and decreased survival rates in B. tabaci nymphs, pseudopupae, and adults. Significant reductions in oviposition duration, fecundity, and hatchability were also observed. Additionally, the metabolic enzyme activity and expression profiles of selected cytochrome P450 monooxygenase (P450) genes following the LC25 treatment of β-asarone suggest that enhanced detoxification via P450s could be involved in the observed sublethal effects. These findings demonstrate the strong toxicity and significant sublethal effects of β-asarone on B. tabaci and suggest that the induced overexpression of P450 genes could be associated with the response to β-asarone.

Neurological disorders are important causes of morbidity and mortality around the world. The increasing prevalence of neurological disorders, associated with an aging population, has intensified the societal burden associated with these diseases, for which no effective treatment strategies currently exist. Therefore, the identification and development of novel therapeutic approaches, able to halt or reverse neuronal loss by targeting the underlying causal factors that lead to neurodegeneration and neuronal cell death, are urgently necessary. Plants and other natural products have been explored as sources of safe, naturally occurring secondary metabolites with potential neuroprotective properties. The secondary metabolites α- and β-asarone can be found in high levels in the rhizomes of the medicinal plant Acorus calamus (L.). α- and β-asarone exhibit multiple pharmacological properties including antioxidant, anti-inflammatory, antiapoptotic, anticancer, and neuroprotective effects. This paper aims to provide an overview of the current research on the therapeutic potential of α- and β-asarone in the treatment of neurological disorders, particularly neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), as well as cerebral ischemic disease, and epilepsy. Current research indicates that α- and β-asarone exert neuroprotective effects by mitigating oxidative stress, abnormal protein accumulation, neuroinflammation, neurotrophic factor deficit, and promoting neuronal cell survival, as well as activating various neuroprotective signalling pathways. Although the beneficial effects exerted by α- and β-asarone have been demonstrated through in vitro and in vivo animal studies, additional research is required to translate laboratory results into safe and effective therapies for patients with AD, PD, and other neurological and neurodegenerative diseases.

This study aims to elucidate the mitigating effects of the volatile oil of (ATR) on dementia, in order to provide a reference for future research and applications of the volatile oil of ATR in the field of dementia. A search strategy was developed using terms such as \"Acori tatarinowii rhizoma,\" \"Acorus tatarinowii Schott,\" \"Asarone,\" and \"Dementia.\" The literature search was conducted in PubMed, Web of Science, and Google Scholar, and studies not meeting the inclusion criteria were excluded. This study summarizes the main metabolites, active ingredients, toxicological properties, and pharmacokinetic characteristics of the volatile oil from ATR in mitigating dementia, with a particular focus on its potential mechanisms of action. Furthermore, the study highlights the limitations of existing research and offers insights into future research directions. The volatile oil of ATR mitigates dementia through multiple pathways, including reducing abnormal protein aggregation, promoting neurogenesis, inhibiting neuronal apoptosis, regulating neurotransmitters, improving synaptic function, modulating autophagy, countering cellular stress, reducing neuroinflammation, and alleviating vascular risk factors. The multi-pathway pharmacological effects of the volatile oil of ATR are well-aligned with the complex mechanisms of dementia progression, highlighting its significant therapeutic potential for anti-dementia applications. This provides new perspectives for the development of more effective anti-dementia drugs. Nonetheless, further rigorous and high-quality preclinical and clinical investigations are required to address key issues, including the chemical characterization of the volatile oil of ATR, potential synergistic effects among active ingredients, toxicity profiles, and definitive clinical efficacy.

β-Asarone (1,2,4-trimethoxy-5-[(Z)-prop-1-enyl]benzene) is an essential component of Acorus tatarinowii Schott volatile oil. Previous research has observed that β-asarone effectively attenuated symptoms in parkinsonian rats and improved their performance, but the mechanism of this effect remains unclear. Other research has shown that endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of Parkinson’s disease (PD). The protein kinase RNA-like endoplasmic reticulum kinase (PERK) was observed in the nigrostriatal dopaminergic neurons of patients with PD. However, our group observed that ER stress and autophagy occurred in 6-hydroxy dopamine (6-OHDA)-induced parkinsonian rats, and ER stress might induce autophagy. We assume that the protective role of β-asarone in parkinsonian rats is mediated via the ER stress-autophagy pathway. To support this hypothesis, we investigated the expressions of glucose regulated protein 78 (GRP78), PERK phosphorylation (p-PERK), C/EBP homologous binding protein (CHOP), Bcl-2 and Beclin-1 in 6-OHDA-induced parkinsonian rats after β-asarone treatment. The results showed that the β-asarone group and PERK inhibitor group had lower levels of GRP78, p-PERK, CHOP and Beclin-1 while having higher levels of Bcl-2. We deduced that β-asarone might regulate the ER stress-autophagy via inhibition of the PERK/CHOP/Bcl-2/Beclin-1 pathway in 6-OHDA-induced parkinsonian rats.

Oxidative stress-mediated neuron damage is considered an important contributor to the pathogenesis and development of neurodegenerative diseases. Although β-asarone is widely known for its neuroprotective pharmacological properties, the exact mechanism of β-asarone against oxidative stress has not been fully elucidated. The aim of the present study was to investigate underlying mechanisms of β-asarone against oxidative damage in PC12 cells. Our results demonstrated that the treatment of β-asarone significantly alleviated the reduction in cell viability and the excessive accumulation of lactate dehydrogenase (LDH), malondialdehyde (MDA) and reactive oxygen species (ROS) by increasing the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH). Moreover, β-asarone pretreatment also activated nuclear factor 2 erythroid-related factor 2 (Nrf2) and its downstream target heme oxygenase-1 (HO-1), which was involved in quenching reactive oxygen to inhibit oxidative stress. Furthermore, when silenced by Nrf2 siRNA, the protective effect of β-asarone was reduced and the oxidative stress induced by H 2 O 2 was enhanced. In conclusion, our findings revealed that β-asarone could reduce oxidative stress via activating Nrf2/HO-1 pathway in PC12 cells, highlighting the potential therapeutic role of β-asarone in neurodegenerative diseases.

Hypoxic injury to the brain is very intricate under the control of biochemical reactions induced by various factors and mechanisms. Long non-coding RNAs (lncRNAs) have already been revealed to affect pathological processes in the nervous system of different degrees. This research aimed to investigate the mechanisms implicated in hypoxic brain injury. β-Asarone mitigated the decrease of cell viability, superoxide dismutase activity, and mitochondrial membrane potential, as well as the increase of cell apoptosis, lactate dehydrogenase release, malondialdehyde content, and reactive oxidative species production by cobalt chloride. LncRNA ribonuclease P RNA component H1 (RPPH1) was discovered to be highly expressed in hypoxia-induced PC12 cells, and β-Asarone addition led to a decline in RPPH1 expression. RPPH1 overexpression reversed the effect of β-Asarone on hypoxia-induced injury in PC12 cells. Furthermore, we proved that RPPH1 could sponge miR-542-3p. Subsequently, death effector domain containing 2 (DEDD2) was proven as the downstream gene of RPPH1/miR-542-3p axis. Eventually, the whole regulation mechanism of RPPH1/miR-542-3p/DEDD2 axis was testified through rescue assays. The impacts of β-Asarone on hypoxia-induced PC12 cells could be countervailed by RPPH1 augment, which was also discovered to be neutralized in response to miR-542-3p overexpression or DEDD2 depletion. These findings offered a novel perspective for understanding neuroprotection.