ArticleNeuropsychiatric disease and treatment2021
Schisandrin Inhibits NLRP1 Inflammasome-Mediated Neuronal Pyroptosis in Mouse Models of Alzheimer's Disease.
Article in Neuropsychiatric disease and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- FA-2-b-β modulates HMGB1/NF-κB/NLRP3 signaling to alleviate neuroinflammation in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- Modulation of programmed cell death by botanical drugs in Alzheimer's disease: a review from a traditional Chinese medicine perspective.Frontiers in pharmacology · 2026Review
- Review
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Pyroptosis: A Novel Therapeutic Target for Bioactive Compounds in Human Disease Treatment? A Narrative Review.Nutrients · 2025Review
- Plant polysaccharides in neuroprotection: mechanistic insights across central nervous system disorders.Frontiers in pharmacology · 2025Review
- Anti-Neuroinflammatory Effects of Adaptogens: A Mini-Review.Molecules (Basel, Switzerland) · 2024Review
- A comprehensive review on Schisandrin and its pharmacological features.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- ZBP1 mediates the progression of Alzheimer's disease via pyroptosis by regulating IRF3.Molecular and cellular biochemistry · 2023Article
- Research Progress on Natural Plant Molecules in Regulating the Blood-Brain Barrier in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Review
- Differential expression of pyroptosis-related genes in the hippocampus of patients with Alzheimer's disease.BMC medical genomics · 2023Article
- Mechanism of pyroptosis in neurodegenerative diseases and its therapeutic potential by traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- To re-examine the intersection of microglial activation and neuroinflammation in neurodegenerative diseases from the perspective of pyroptosis.Frontiers in aging neuroscience · 2023Review
- The role of pyroptosis in cognitive impairment.Frontiers in neuroscience · 2023Review
- Article
- Pyroptosis as a candidate therapeutic target for Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Caspase-1 and Gasdermin D Afford the Optimal Targets with Distinct Switching Strategies in NLRP1b Inflammasome-Induced Cell Death.Research (Washington, D.C.) · 2022Article
- Schizandrin A ameliorates cognitive functions via modulating microglial polarisation in Alzheimer's disease mice.Pharmaceutical biology · 2021Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIn recent years, schisandrin (SCH) was proved to improve Alzheimer's Disease (AD). The aim of our study is to explore the effect of SCH on neuronal pyroptosis in the disease.
methodsA Morris water maze test was performed to evaluate the spatial learning and memory retention of AD mouse. ELISA was fulfilled to examine the concentration of Aβ, IL-1β, and IL-18. Western blot was performed to detect the expression of apoptosis- and pyroptosis-related proteins. Besides, the neuronal apoptosis rate was examined using TUNEL assay. Immunohistochemistry was utilized to detect the activation of NLRP1 inflammasome.
resultsHere, AD mice have serious cognitive impairment. Meantime, Aβ was highly expressed in the brains of AD mice. SCH could effectively rescue the cognitive impairment in AD mice and impede the production of Aβ. Subsequently, we further demonstrated that SCH repressed neuronal apoptosis, pyroptosis-related proteins expression, and the activation of NLRP1 inflammasome in the hippocampus of AD mice. We also proved that Aβ induced neuronal apoptosis and pyroptosis in vitro. However, the effects of Aβ on neuronal apoptosis and pyroptosis were partly reversed by SCH treatment.
conclusionOverall, our data indicated that SCH improved cognitive impairment in AD mice through inhibition of NLRP1 inflammasome-mediated neuronal pyroptosis and neuronal apoptosis. Our works provided new evidence to support SCH acting as a potential treatment method in AD.
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