Polygala tenuifolia (PT), Magnolia officinalis (MO), and their combination (PM) can each alleviate cognitive decline in a mouse model of .
PT, MO, and PM reduce neuropathological damage in D-gal mice to varying degrees.
Each treatment lowers the levels of pro-inflammatory factors in both serum and hippocampal tissue.
PM increases levels of antioxidant markers, specifically superoxide dismutase (SOD) and glutathione (GSH).
Network pharmacology and experimental validation indicate that PM enhances the expression of tight junctions and proteins in the cAMP pathway while inhibiting the NF-κB pathway.
PM corrects gut microbiota imbalances by increasing the abundance of short-chain fatty acid-producing bacteria and decreasing LPS-producing bacteria.
Simplified
PURPOSE: Willd. (PT) is commonly used to address (CI), whileRehd. et Wils (MO) is often prescribed for gastrointestinal issues as well as CI. This study seeks to explore the impacts and mechanisms behind the combined therapy of PT and MO (PM) in treating CI, based on the concept of the . Polygala tenuifolia Magnolia officinalis
METHODS: The characteristic components of PT, MO, and PM were identified using ultra-high performance liquid chromatography-tandem triple quadrupole mass Spectrometry (UPLC-MS/MS). A mouse model was established by D-gal induction, and the effects of PT, MO, and PM on CI were evaluated through behavioral tests, pathological staining, and Enzyme-Linked Immunosorbent Assay (ELISA). Subsequently, network pharmacology was used to analyze the potential mechanisms by which PM improves CI, followed by validation through Western blotting (WB), traditional Chinese medicine (TEM), Immunofluorescence (IF), and 16S rRNA.
RESULTS: PT, MO, and PM can each alleviate cognitive decline and neuropathological damage in D-gal mice to varying degrees, reduce the expression of pro-inflammatory factors (TNF-α, IL-1β, IL-6, IFN-γ, LPS) in serum or hippocampal tissue, and increase SOD and GSH levels. Network pharmacology analysis and molecular experiments confirmed that PM upregulates the expression of tight junction s (TJs), enhances the expression of proteins in the cAMP pathway, and inhibits p-NF-κB-p65 expression. PM reverses D-gal-induced gut microbiota dysbiosis, increases the abundance of SCFA-producing bacteria, and decreases the abundance of LPS-producing bacteria.
CONCLUSION: PM alleviates CI by reducing inflammation and oxidative stress, protecting the blood-brain barrier (BBB) and intestinal barrier, inhibiting the NF-κB pathway, activating the cAMP pathway, and regulating gut microbiota.
Key numbers
TNF-α, IL-1β, IL-6, IFN-γ levels
Decrease in Pro-Inflammatory Cytokines
Levels in serum and hippocampus of D-gal-treated mice.
Not specified
Increase in SCFA-Producing Bacteria
Changes in gut microbiota composition post-PM treatment.
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