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Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
Astragaloside's Role in Microglial Neuroinflammation: A Multi-Method Study Combining Experimental and Computational
Dian Ou1, Jiating Li1, Yiming Shi1
1Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine On Prevention And Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China.
Abstract:
This study investigates the mechanism by which astragaloside (AST) modulates microglial metabolism to alleviate inflammatory injury following oxygen-glucose deprivation/reoxygenation (OGD/R), a model simulating ischemic brain injury. Four groups were studied: Control, Model, AST-treated, and Positive Control (NBP). Cell injury was assessed via CCK-8 assay, and microglial M1 polarization was analyzed by flow cytometry. TNF-α and IL-1β protein levels were measured using ELISA, while IL-1β and IL-10 mRNA expression was quantified by PCR. Core targets were identified through network pharmacology, followed by GO/KEGG enrichment analysis and molecular docking. Protein expression was validated by Western blotting, and metabolic changes were evaluated via metabolomics. AST significantly attenuated OGD/R-induced microglial injury, suppressed TNF-α and IL-1β expression, and inhibited M1 polarization while upregulating IL-10 mRNA. Network pharmacology and molecular docking revealed AST's strong binding affinity to key energy metabolism proteins, including SRC, AKT, and mTOR. Western blotting confirmed activation of SRC and AKT pathways. Metabolomics indicated that AST reversed OGD/R-induced metabolic shifts, downregulating linoleic acid metabolism while modulating glycerophospholipid and pentose phosphate pathways. Astragaloside mitigates OGD/R-induced inflammatory injury by modulating SRC and AKT signaling pathways, leading to metabolic reprogramming in microglia. These findings highlight AST's potential as a therapeutic agent for neuroinflammatory disorders.
Insights
Astragaloside (AST) protects against brain injury by regulating microglial metabolism and reducing inflammation. This natural compound shows promise for treating neuroinflammatory disorders.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Ischemic brain injury, modeled by oxygen-glucose deprivation/reoxygenation (OGD/R), triggers microglial inflammatory responses.
- Microglial metabolic reprogramming plays a critical role in OGD/R-induced inflammatory injury.
- Astragaloside (AST), a compound from Astragalus, is explored for its therapeutic potential.
Purpose of the Study:
- To elucidate the mechanism by which astragaloside (AST) modulates microglial metabolism to alleviate inflammatory injury following OGD/R.
- To investigate AST's effects on microglial polarization and inflammatory mediator release.
- To identify the molecular targets and signaling pathways affected by AST.
Main Methods:
- Cell injury assessed by CCK-8 assay; microglial M1 polarization by flow cytometry.
- Inflammatory markers (TNF-α, IL-1β, IL-10) measured by ELISA and PCR.
- Network pharmacology, molecular docking, Western blotting, and metabolomics used to identify targets and pathways.
Main Results:
- AST significantly reduced OGD/R-induced microglial injury and inflammatory cytokine expression (TNF-α, IL-1β).
- AST inhibited M1 microglial polarization and increased anti-inflammatory IL-10 mRNA.
- Network pharmacology identified SRC, AKT, and mTOR as key targets; AST modulated SRC/AKT pathways and reversed metabolic shifts.
Conclusions:
- Astragaloside mitigates OGD/R-induced inflammatory brain injury by reprogramming microglial metabolism via SRC and AKT signaling.
- AST demonstrates potential as a therapeutic agent for neuroinflammatory diseases like ischemic stroke.
