Primary Investigation for the Mechanism of Biatractylolide from <i>Atractylodis Macrocephalae Rhizoma</i> as an Acetylcholinesterase Inhibitor

Xie, Ying; Ning, Ning; Zhu, Linghua; Dan-ning, LI; Feng, Xing; Yang, Xiao‐Ping

doi:10.1155/2016/7481323

Cited by 7 publications

(6 citation statements)

References 24 publications

(25 reference statements)

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“…Our previous study confirmed that biatractylolide has a significant effect on reducing the activity of AChE in the brain and improving the memory ability of mouse dementia induced by aluminum trichloride [ 18 ]; moreover, biatractylolide can significantly reduce cholinesterase activity in model rats and improve the behavior and memory of AD model rats induced by A β 1−40 [ 19 ]. Importantly, biatractylolide can inhibit the enzyme activity of AChE and downregulate the expression of AChE in a dose-dependent manner, which has been confirmed in our previous study [ 20 ]. However, the specific mechanisms of biatractylolide are not well understood, and there are no reports about protective effect of biatractylolide currently.…”

Section: Introductionsupporting

confidence: 83%

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Biatractylolide Modulates PI3K‐Akt‐GSK3β‐Dependent Pathways to Protect against Glutamate‐Induced Cell Damage in PC12 and SH‐SY5Y Cells

Zhu

Ning

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Biatractylolide, isolated from the ethyl acetate extract of Atractylodes macrocephala, has shown various pharmacological activities such as antitumor and antioxidant activities. In this work, we aim to study the protective effect of biatractylolide on glutamate-induced rat adrenal pheochromocytoma cell (PC12) and human bone marrow neuroblastoma cell line (SH-SY5Y) injury and preliminarily explore its mechanism. The results showed that glutamate was cytotoxic with an inhibitory concentration 50% (IC50) of 8.5 mM in PC12 and 10 mM in SH-SY5Y cells. In this work, the preincubation with biatractylolide (10, 15, and 20 μM) observably improved cell viability, inhibited the apoptosis of cells induced by glutamate, and reduced the activity of LDH. AO staining revealed that apoptosis of cells was decreased. Additionally, the results of western blotting manifested that pretreatment with biatractylolide could downregulate GSK3β protein expression and upregulate p-Akt protein expression, thereby protecting PC12 and SH-SY5Y cells from injury. All these findings indicate that biatractylolide has a neuroprotective effect on glutamate-induced injury in PC12 and SH-SY5Y cells through a mechanism of the PI3K-Akt-GSK3β-dependent pathways.

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Section: Introductionsupporting

confidence: 83%

“…Biatractylolide was isolated from the ethyl acetate extract of Atractylodes macrocephala by multistep chromatographic processing [ 20 ] ( Figure 1 ). Glutamate and DMSO were purchased from Sigma Chemicals (USA).…”

Section: Methodsmentioning

confidence: 99%

Biatractylolide Modulates PI3K‐Akt‐GSK3β‐Dependent Pathways to Protect against Glutamate‐Induced Cell Damage in PC12 and SH‐SY5Y Cells

Zhu

Ning

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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“…This small molecule has a symmetrical structure containing a novel double sesquiterpene ester. Xie et al (2016) showed that biatractylolide (C30) had a significant effect on inhibiting the activity of AChE in the brain and improved the memory ability of dementia mouse induced by aluminum trichlo-ride. The IC50 values of inhibiting AChE activity is 6.55 µM and its molecular mechanisms includes not only binding to AChE but also reducing AChE expression by inhibiting the activity of glycogen synthase kinase (GSK) 3.…”

Section: Non-alkaloidsmentioning

confidence: 99%

“…The underlying mechanism is an increased expression of PP1 and PP2A, increased phosphorylation of PI3K (p85) and Akt (Ser473) and decreased phosphorylation of GSK3β (tyr216), leading to a reduced level of tau phosphorylation (Liu et al, 2014). Xie et al (2016) demonstrated that biatractylolide (C30) could strongly inhibit AChE activity with an IC50 value of 6.5458 µM. The underlying molecular mechanisms are not only binding to AChE but also reduced AChE expression by inhibition of GSK3 activity.…”

Section: Terpenoidsmentioning

confidence: 99%

Current anti-Alzheimer's disease effect of natural products and their principal targets

2019

Journal of Integrative Neuroscience

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Various bioactive substances isolated from natural products play a pivotal role in the prevention and cure of neurodegenerative diseases, such as Alzheimer's disease. Currently, there are many theories about the pathogenesis of this disease. In this review we discuss among them, the cholinergic hypotheses, the Aβ toxicity hypothesis, and the tau dysfunction hypothesis. Multiple potential targets are a focus for the development of anti-AD drugs. There is an urgent need to develop more effective therapies to treat and delay the onset of the disease and to find safe and effective drugs. In this review, the recent progress of anti-AD effects and their principal targets are updated.

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“…It could significantly reduce acetylcholinesterase activity in a rat AD model induced by Aβ 1-40 and improve behavior and memory. Therefore, BD showed promising potential to be an effective anti-AD drug [ 44 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of the Psychoactive Compound Biatractylolide (BD) in Alzheimer’s Disease

Wang

Irshad

et al. 2022

Molecules

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Mitochondria play a central role in the survival or death of neuronal cells, and they are regulators of energy metabolism and cell death pathways. Many studies support the role of mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer’s disease. Biatractylolide (BD) is a kind of internal symmetry double sesquiterpene novel ester compound isolated from the Chinese medicinal plant Baizhu, has neuroprotective effects in Alzheimer’s disease. We developed a systematic pharmacological model based on chemical pharmacokinetic and pharmacological data to identify potential compounds and targets of Baizhu. The neuroprotective effects of BD in PC12 (rat adrenal pheochromocytoma cells) and SH-SY5Y (human bone marrow neuroblastoma cells) were evaluated by in vitro experiments. Based on the predicted results, we selected 18 active compounds, which were associated with 20 potential targets and 22 signaling pathways. Compound-target, target-disease and target-pathway networks were constructed using Cytoscape 3.2.1. And verified by in vitro experiments that BD could inhibit Aβ by reducing oxidative stress and decreasing CytC release induced mPTP opening. This study provides a theoretical basis for the development of BD as an anti-Alzheimer’s disease drug.

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Primary Investigation for the Mechanism of Biatractylolide from Atractylodis Macrocephalae Rhizoma as an Acetylcholinesterase Inhibitor

Cited by 7 publications

References 24 publications

Biatractylolide Modulates PI3K‐Akt‐GSK3β‐Dependent Pathways to Protect against Glutamate‐Induced Cell Damage in PC12 and SH‐SY5Y Cells

Biatractylolide Modulates PI3K‐Akt‐GSK3β‐Dependent Pathways to Protect against Glutamate‐Induced Cell Damage in PC12 and SH‐SY5Y Cells

Current anti-Alzheimer's disease effect of natural products and their principal targets

Neuroprotective Effects of the Psychoactive Compound Biatractylolide (BD) in Alzheimer’s Disease

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