ArticlePloS one2022
Ganoderma tsugae prevents cognitive impairment and attenuates oxidative damage in d-galactose-induced aging in the rat brain.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- β-Asarone, Tenuifolin, and YuanZhi Decoction Restore Cognitive Function and Modulate GRIN2B-Associated Autophagy in Alzheimer's Disease.Neurochemical research · 2026Article
- Phytochemical and Fungal Bioactive Compounds in the "Brain Health Triad": A Narrative Review on Neurostimulating, Neurotrophic, and Neuroprotective Synergy.International journal of molecular sciences · 2026Review
- Evaluation of Two Different Treatments for Larch Logs as Substrates to CultivateLife (Basel, Switzerland) · 2024Article
- Ganoderma tsuage promotes pain sensitivity in aging mice.Scientific reports · 2024Article
- Diosgenin alleviates D-galactose-induced oxidative stress in rats' brain and liver targeting aging and apoptotic marker genes.Frontiers in molecular biosciences · 2024Article
- Improved Solubility and Activity of Natural Product in Nanohydrogel.Pharmaceuticals (Basel, Switzerland) · 2023Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lingzhi has long been regarded as having life-prolonging effects. Research in recent years has also reported that Lingzhi possesses anti-tumor, anti-inflammatory, immunomodulatory, hepatoprotective, and anti-lipogenic effects. The D-galactose (D-gal, 100 mg/kg/day)-induced aging Long-Evans rats were simultaneously orally administered a DMSO extract of Ganoderma tsugae (GTDE, 200 μg/kg/day) for 25 weeks to investigate the effects of GTDE on oxidative stress and memory deficits in the D-galactose-induced aging rats. We found that GTDE significantly improved the locomotion and spatial memory and learning in the aging rats. GTDE alleviated the aging-induced reduction of dendritic branching in neurons of the hippocampus and cerebral cortex. Immunoblotting revealed a significant increase in the protein expression levels of the superoxide dismutase-1 (SOD-1) and catalase, and the brain-derived neurotrophic factor (BDNF) in rats that received GTDE. D-gal-induced increase in the lipid peroxidation product 4-hydroxynonenal (4-HNE) was significantly attenuated after the administration of GTDE, and pyrin domain-containing 3 protein (NLRP3) revealed a significant decrease in NLRP3 expression after GTDE administration. Lastly, GTDE significantly reduced the advanced glycosylation end products (AGEs). In conclusion, GTDE increases antioxidant capacity and BDNF expression of the brain, protects the dendritic structure of neurons, and reduces aging-induced neuronal damage, thereby attenuating cognitive impairment caused by aging.
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