Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Ethnopharmacological Relevance: Polygalae Radix has high pharmacological activity and has been widely used as a sedative and tranquilizer to increase cognitive function, prevent epilepsy, and treat respiratory diseases such as bronchitis. However, its role in delaying aging and decreasing oxidative stress and its main functional factors have not been thoroughly studied.
Aim Of The Study: The purpose was to investigate the antiaging and antioxidant effects of aqueous Polygalae Radix extract (PRE) and its mechanism of action.
Materials And Methods: The effects of different concentrations (1, 5, and 10 mg/mL) of PRE on the lifespan, body length, reproductive ability, motility, lipofuscin, and reactive oxygen species (ROS) on a model of natural senescence of Caenorhabditis elegans were investigated. The effects of PRE treatment on the expression of body weight, malondialdehyde (MDA), glutathione peroxidase (GSH-PX), and mTERT content were evaluated in a D-galactose (Dgal)-induced mouse model of aging. Histopathological changes in the liver and brain of mice were analyzed by hematoxylin-eosin (HE). The enriched pathways associated with differentially expressed genes in the liver tissues of C. elegans and mice were analyzed via RNA-seq, and the results were verified via RT-qPCR, cell transfection and Western blotting. Abundance of and changes in the mouse intestinal flora were analyzed by 16S rDNA sequencing.
Results: PRE significantly prolonged the average lifespan of C. elegans and improved the physiological indices related to senescence. In addition, PRE slowed the decrease in weight of senescent model mice; protected serum, liver and brain tissues from oxidative stress damage; increased GSH-PX expression; and reduced MDA expression. The role of PRE in the low- and middle-dose groups was similar to that of vitamin C (VC) in inhibiting oxidative stress, but the effect of PRE in the high-dose group was greater than that of VC. The RNA-seq results suggested that PRE might be related to PPARγ/MAPK, and the subsequent RT-qPCR and cell transfection results indicated that PRE decreased oxidative stress by downregulating the mRNA expression of the Fabp1, Acaa1b, Hmgcs1, Map3K5, and Rac2 genes. The Western blot results revealed that PRE decreased oxidative stress by increasing PPARγ expression and inhibiting p38 protein phosphorylation. 16S rDNA sequencing showed that PRE treatment increased the abundance of the intestinal flora in mice and inhibited the growth of pathogenic bacteria such as Helicobacter pylori and Desulfurization vibrio while promoting the growth of beneficial bacteria such as Bifidobacteria.
Conclusions: PRE delays aging and resists oxidative stress in organisms; it may act by regulating the PPARγ/MAPK signaling pathway and the intestinal flora. The efficacy and mechanism of PRE against oxidative stress were elucidated using RNA-seq and 16S rDNA sequencing, providing a reference for antiaging and aging-related diseases.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jep.2025.119878 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Guishen-erxian Decoction can improve ovarian function in rats with premature ovarian failure by inhibiting oxidative stress and granulosa cell DNA fragmentation mediated by the PI3K/Akt/FOXO3a pathway.
Histol Histopathol
September 2025
Center for Experimental Teaching, School of Pharmacy, Guangzhou Medical University, Guangzhou, China.
Background: The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.
Method: The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.
SIRT3-FOXO3a Isoforms Forge Nuclear-Mitochondrial Links to Combat Sepsis-Induced Cardiomyopathy Oxidative Stress in Mice.
Antioxid Redox Signal
September 2025
Department of Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Sepsis-induced cardiomyopathy (SIC) is a serious complication of sepsis. The relationship between SIC and protein acetylation, particularly the balance between acetylation and deacetylation in cardiomyocyte subcellular structures, as well as how nuclear-mitochondrial coordination maintains standard antioxidant stress capacity, remains unclear. This study focused on exploring the nuclear-mitochondrial regulatory mechanisms formed by the interplay of Sirtuin 3 (SIRT3) and Forkhead box O3a (FOXO3a).
View Article and Find Full Text PDFConcussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.
Lab Chip
September 2025
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA.
Traumatic brain injuries (TBIs) are a risk factor for Alzheimer's disease (AD), and share several important pathological features including the development of neurofibrillary tangles (NFT) of tau protein. While this association is well established, the underlying pathogenesis is poorly defined and current treatment options remain limited, necessitating novel methods and approaches. In response we developed "TBI-on-a-chip", an trauma model utilizing murine cortical networks on microelectrode arrays (MEAs), capable of reproducing clinically relevant impact injuries while providing simultaneous morphological and electrophysiological readout.
View Article and Find Full Text PDFType-I Supramolecular Photosensitizer Enables GSH Depletion by Hydrogen Atom Transfer.
J Am Chem Soc
September 2025
Key Laboratory of Radiopharmaceuticals, Ministry of Education, College of Chemistry, Beijing Normal University, Beijing 100875, P. R. China.
Photodynamic therapy (PDT) induces oxidative stress that triggers a compensatory upregulation of intracellular glutathione (GSH), thereby diminishing PDT efficacy. The simultaneous generation of reactive oxygen species and depletion of GSH holds promise for amplifying oxidative damage and enhancing therapeutic outcomes yet remains a challenge. In this work, we present a Type-I supramolecular photosensitizer designed to deplete GSH through a hydrogen atom transfer mechanism while concurrently generating superoxide radicals.
View Article and Find Full Text PDFMitochondrial ClpX Inhibition Induces Ferroptosis and Blocks Pancreatic Cancer Cell Proliferation.
Chembiochem
September 2025
School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, 310024, P. R. China.
The ATPase caseinolytic protease X (ClpX), forming the ClpXP complex with caseinolytic protease P (ClpP), is essential for mitochondrial protein homeostasis. While ClpP targeting is a recognized anticancer strategy, the role of ClpX in cancer remains underexplored. In pancreatic ductal adenocarcinoma (PDAC), elevated CLPX expression correlates with poor prognosis, suggesting its oncogenic function.
View Article and Find Full Text PDF