ArticlePloS one2014
Protective effects of astragaloside IV against amyloid beta1-42 neurotoxicity by inhibiting the mitochondrial permeability transition pore opening.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Supplementation with Curcuma longa Reverses Neurotoxic and Behavioral Damage in Models of Alzheimer's Disease: A Systematic Review.Current neuropharmacology · 2019Pooled it
- Astragaloside IV Supplementation Promotes A Neuroprotective Effect in Experimental Models of Neurological Disorders: A Systematic Review.Current neuropharmacology · 2019Pooled it
- Efficacy of Shenqi Pollen Capsules for High-Altitude Deacclimatization Syndrome via Suppression of the Reoxygenation Injury and Inflammatory Response.Journal of immunology research · 2019Trial
- Mechanistic convergence ofIBRO neuroscience reports · 2026Article
- Review
- Exploring the Neuroprotective Potential ofBiomolecules · 2025Review
- Neuroprotective Role of Piperine-Encapsulated Casein Micelles in Mitigating Intracellular Dyshomeostasis in Alzheimer's Disease Pathology.Molecular neurobiology · 2025Article
- RoastedAntioxidants (Basel, Switzerland) · 2025Article
- A Pilot EEG Study on the Acute Neurophysiological Effects of Single-Dose Astragaloside IV in Healthy Young Adults.Nutrients · 2025Article
- Astragaloside IV reduces mutant Ataxin-3 levels and supports mitochondrial function in Spinocerebellar Ataxia Type 3.Scientific reports · 2024Article
- Efficacy, safety, and response predictors of Astragalus in patients with mild to moderate Alzheimer's disease: A study protocol of an assessor-blind, statistician-blind open-label randomized controlled trial.Contemporary clinical trials communications · 2024Article
- Article
- Roles and Mechanisms of Astragaloside IV in Combating Neuronal Aging.Aging and disease · 2022Review
- Exercise Rehabilitation and/or Astragaloside Attenuate Amyloid-beta Pathology by Reversing BDNF/TrkB Signaling Deficits and Mitochondrial Dysfunction.Molecular neurobiology · 2022Article
- Medicine-Food Herbs against Alzheimer's Disease: A Review of Their Traditional Functional Features, Substance Basis, Clinical Practices and Mechanisms of Action.Molecules (Basel, Switzerland) · 2022Review
- Current Progress on Neuroprotection Induced by Artemisia, Ginseng, Astragalus, and Ginkgo Traditional Chinese Medicines for the Therapy of Alzheimer's Disease.Oxidative medicine and cellular longevity · 2022Review
- Review
- Asymptomatic neurotoxicity of amyloid β-peptides (Aβ1-42 and Aβ25-35) on mouse embryonic stem cell-derived neural cells.Bosnian journal of basic medical sciences · 2021Article
- Protective Effects and Mechanisms ofBehavioural neurology · 2021Article
- Astragaloside IV Protects 6-Hydroxydopamine-Induced SH-SY5Y Cell Model of Parkinson's Disease via Activating the JAK2/STAT3 Pathway.Frontiers in neuroscience · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction caused by amyloid β-peptide (Aβ) plays an important role in the pathogenesis of Alzheimer disease (AD). Substantial evidence has indicated that the mitochondrial permeability transition pore (mPTP) opening is involved in Aβ-induced neuronal death and reactive oxygen species (ROS) generation. Astragaloside IV (AS-IV), one of the major active constituents of Astragalus membranaceus, has been reported as an effective anti-oxidant for treating neurodegenerative diseases. However, the molecular mechanisms still need to be clarified. In this study, we investigated whether AS-IV could prevent Aβ1-42-induced neurotoxicity in SK-N-SH cells via inhibiting the mPTP opening. The results showed that pretreatment of AS-IV significantly increased the viability of neuronal cells, reduced apoptosis, decreased the generation of intracellular reactive oxygen species (ROS) and decreased mitochondrial superoxide in the presence of Aβ1-42. In addition, pretreatment of AS-IV inhibited the mPTP opening, rescued mitochondrial membrane potential (ΔΨm), enhanced ATP generation, improved the activity of cytochrome c oxidase and blocked cytochrome c release from mitochondria in Aβ1-42 rich milieu. Moreover, pretreatment of AS-IV reduced the expression of Bax and cleaved caspase-3 and increased the expression of Bcl-2 in an Aβ1-42 rich environment. These data indicate that AS-IV prevents Aβ1-42-induced SK-N-SH cell apoptosis via inhibiting the mPTP opening and ROS generation. These results provide novel insights of AS-IV for the prevention and treatment of neurodegenerative disorders such as AD.
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