ArticleBMC complementary medicine and therapies2024
Panax notoginseng saponins prevent dementia and oxidative stress in brains of SAMP8 mice by enhancing mitophagy.
Article in BMC complementary medicine and therapies, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Circular RNA circTrpc6-induced tau phosphorylation contributes to neuronal injury and cognitive decline via miR-485-5p/eIF4E axis in senescence-accelerated mouse prone 8 mice.Cell biology and toxicology · 2026Article
- Yixin Yangshen Granules Target HIF-1 Signaling to Modulate the Neuroimmune Microenvironment in Alzheimer's Disease: Insights from Integrative Multi-Omics and Deep Learning.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Role of Saponins fromMolecules (Basel, Switzerland) · 2025Article
- The role of Panax notoginseng saponins in cerebrovascular neurological disorders: an overview of mechanisms and functions.Frontiers in pharmacology · 2025Review
- Olive Oil Industry By-Products as a Novel Source of Biophenols with a Promising Role in Alzheimer Disease Prevention.Molecules (Basel, Switzerland) · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMitochondrial dysfunction is one of the distinctive features of neurons in patients with Alzheimer's disease (AD). Intraneuronal autophagosomes selectively phagocytose and degrade the damaged mitochondria, mitigating neuronal damage in AD. Panax notoginseng saponins (PNS) can effectively reduce oxidative stress and mitochondrial damage in the brain of animals with AD, but their exact mechanism of action is unknown.
methodsSenescence-accelerated mouse prone 8 (SAMP8) mice with age-related AD were treated with PNS for 8 weeks. The effects of PNS on learning and memory abilities, cerebral oxidative stress status, and hippocampus ultrastructure of mice were observed. Moreover, changes of the PTEN-induced putative kinase 1 (PINK1)-Parkin, which regulates ubiquitin-dependent mitophagy, and the recruit of downstream autophagy receptors were investigated.
resultsPNS attenuated cognitive dysfunction in SAMP8 mice in the Morris water maze test. PNS also enhanced glutathione peroxidase and superoxide dismutase activities, and increased glutathione levels by 25.92% and 45.55% while inhibiting 8-hydroxydeoxyguanosine by 27.74% and the malondialdehyde production by 34.02% in the brains of SAMP8 mice. Our observation revealed the promotion of mitophagy, which was accompanied by an increase in microtubule-associated protein 1 light chain 3 (LC3) mRNA and 70.00% increase of LC3-II/I protein ratio in the brain tissues of PNS-treated mice. PNS treatment increased Parkin mRNA and protein expression by 62.80% and 43.80%, while increasing the mRNA transcription and protein expression of mitophagic receptors such as optineurin, and nuclear dot protein 52.
conclusionPNS enhanced the PINK1/Parkin pathway and facilitated mitophagy in the hippocampus, thereby preventing cerebral oxidative stress in SAMP8 mice. This may be a mechanism contributing to the cognition-improvement effect of PNS.
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