ArticleChinese journal of integrative medicine2018
Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson's Disease.
Article in Chinese journal of integrative medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Prophylactic effects ofBiomedical reports · 2026Article
- Therapeutic potential of neuroprotective plant extracts in Parkinson's disease.Frontiers in neuroscience · 2026Review
- Study on the Mechanism of Acanthopanax senticosus Extract Intervening in the Regulation of Parkinson's Disease by BV2 Microglial Cell-Derived Exosomes.Molecular neurobiology · 2025Article
- Spatial metabolomics reveals the effects of Acanthopanax senticosus on region-specific alterations in neurotransmitters and metabolites levels in the brains of α-syn transgenic Parkinson's disease model mice.Metabolic brain disease · 2025Article
- Deficient AMPK-SENP1-Sirt3 signaling impairs mitochondrial complex I function in Parkinson's disease model.Translational neurodegeneration · 2025Article
- Study on the protective effects and mechanisms of eleutherococcus senticosus on korsakoff syndrome.Frontiers in neuroscience · 2025Review
- Review
- A critical appraisal on the involvement of plant-based extracts as neuroprotective agents (2012-2022): an effort to ease out decision-making process for researchers.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- A review of the extraction and purification methods, biological activities, and applications of active compounds inFrontiers in nutrition · 2024Review
- Feasibility and Safety of Food ContainingPalliative medicine reports · 2024Article
- Neuroprotective effects of morroniside from Cornus officinalis sieb. Et zucc against Parkinson's disease via inhibiting oxidative stress and ferroptosis.BMC complementary medicine and therapies · 2023Article
- Article
- Dietary supplementation ofFrontiers in nutrition · 2023Article
- Mitochondrial dysfunction-targeting therapeutics of natural products in Parkinson's disease.Frontiers in pharmacology · 2023Review
- Role of traditional Chinese medicine in ameliorating mitochondrial dysfunctionFrontiers in pharmacology · 2023Review
- Integrated network pharmacology and hepatic metabolomics to reveal the mechanism ofFrontiers in cell and developmental biology · 2022Article
- A Novel Method for Identifying Parkin Binding Agents in Complex Preparations of Herbal Medicines.Oxidative medicine and cellular longevity · 2022Article
- Protective Effects of Hu-Lu-Ba-Wan () against Oxidative Stress in Testis of Diabetic Rats through PKCα/NAPDH Oxidase Signaling Pathway.Chinese journal of integrative medicine · 2021Article
- Acanthopanax senticosus Harms extract causes G0/G1 cell cycle arrest and autophagy via inhibition of Rubicon in human liver cancer cells.Oncology reports · 2021Article
- Targeting PINK1 Using Natural Products for the Treatment of Human Diseases.BioMed research international · 2021Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the neuro-protective effects of Acanthopanax senticosus Harms (EAS) on mesencephalic mitochondria and the mechanism of action, using a mouse model of Parkinson's disease (PD).
methodsThe chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms (EAS) was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group, the MPTP model group, and the EAS treated group with MPTP (MPTP+EAS group, 10 in each group). The MPTP model group and the MPTP+EAS group received MPTP-HCl (30 mg/kg i.p) once a day for 5 days. The control group received an equal volume of saline (20 mL/kg i.p) once a day for 5 days. Induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride daily (MPTP-HCl, 30 mg/kg) for 5 days, the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model, including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1 (MT-ND1), succinate dehydrogenase complex subunit A (SDHA), and succinate dehydrogenase cytochrome b560 subunit (SDHC).
resultsAfter treatment with EAS, the behavioral changes induced by MPTP were attenuated significantly (P<0.05). EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential (both P<0.05), which was supported by an ultra-structural level analysis. The changes in reactive oxygen species (ROS), malonic dialdehyde (MDA), oxidative phosphorylation (OXPHOS) system 4 subunits levels and PD-related proteins expressions (parkin, Pink1, DJ-1, α-synuclein, and Lrrk2) reverted to near normal levels (all P<0.05), based on the results of immune-histological and Western blotting observations.
conclusionsThe neuro-protective effects of EAS are linked to protecting mice against MPTP-induced mitochondrial dysfunction and structural damage. Therefore, EAS is a promising candidate for the prevention or treatment of mitochondrial neurodegenerative disorders, such as PD.
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