ArticleAging2024
Gastrodin ameliorates neuroinflammation in Alzheimer's disease mice by inhibiting NF-κB signaling activation via PPARγ stimulation.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Gastrodin Ameliorates Blood Pressure by Targeting the PPAR-γ/NF-κB/NLRP3 Signaling Axis in the Hypothalamic Paraventricular Nucleus.Cardiovascular toxicology · 2026Article
- Article
- Gastrodin alleviates cardiomyocyte senescence by regulating autophagy through the AMPK/mTOR/4EBP1 pathway.Frontiers in pharmacology · 2026Article
- Ginsenoside RK1 inhibits microglial activation and ROS production and alleviates vascular dementia in rats.Journal of clinical biochemistry and nutrition · 2025Article
- Gastrodin Alleviates Tau Pathology by Targeting the Alzheimer's Risk Gene FERMT2, Reversing the Reduction in Brain Viscoelasticity.CNS neuroscience & therapeutics · 2025Article
- Natural Products from Chinese Medicine Targeting NF-κB Signaling: Emerging Therapeutic Avenues for Neurodegenerative Diseases.Drug design, development and therapy · 2025Review
- Combined administration of catalpol, puerarin, gastrodin, and borneol modulates the Tlr4/Myd88/NF-κB signaling pathway and alleviates microglia inflammation in Alzheimer's disease.Frontiers in pharmacology · 2024Article
- A New Frontier in Phytotherapy: Harnessing the Therapeutic Power of Medicinal Herb-derived miRNAs.Current pharmaceutical design · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimWe investigated the effects and targets of gastrodin (GAS) for improving cognitive ability in Alzheimer's disease (AD).
methodsThe targets and mechanisms of GAS were analyzed by network pharmacology. Morris water and eight-arm radial mazes were used to detect the behaviors of 7-months-old APP/PS1 mice. The levels of IBA-1 and PPARγ were examined by histochemical staining, nerve cells were detected by Nissl staining, inflammatory cytokines were measured by ELISA, and protein expressions were monitored by Western blotting. The neurobehavioral effects of GAS on mice were detected after siRNA silencing of PPARγ. Microglia were cultured
resultsNetwork pharmacological analysis revealed that PPARγ was the action target of GAS. By stimulating PPARγ, GAS inhibited NF-κB signaling activation and decreased neuroinflammation and microglial activation, thereby ameliorating the cognitive ability of AD mice. After silencing PPARγ, GAS could not further improve such cognitive ability. Cellular-level results demonstrated that GAS inhibited microglial injury, reduced tissue inflammation, and activated PPARγ.
conclusionsGAS can regulate microglia-mediated inflammatory response by stimulating PPARγ and inhibiting NF-κB activation, representing a mechanism whereby it improves the cognitive behavior of AD.
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