Panax ginseng, a foundational herb in traditional East Asian medicine, has been extensively studied for its therapeutic and nutritional properties. Among its bioactive constituents, ginseng polysaccharides (GPs) stand out for their potent antioxidant, anti-inflammatory, and immunomodulatory effects. These polysaccharides, primarily composed of monosaccharides such as glucose, galactose (Gal), and arabinose (Ara), demonstrate promising potential in alleviating oxidative stress and immune suppression. With increasing exposure to ionizing radiation from medical and industrial sources, the demand for effective radioprotective agents has grown. Ionizing radiation induces DNA damage and excessive reactive oxygen species (ROS) production, resulting in oxidative stress and immune dysfunction. Research suggests that GPs mitigate radiation-induced cellular damage by enhancing antioxidant enzyme activity, suppressing inflammatory cytokines, and regulating immune responses. Despite these encouraging findings, further investigations are needed to elucidate their mechanisms of action and optimize their clinical applications. This review provides a comprehensive analysis of the composition, biological activities, and radioprotective mechanisms of GPs, highlighting their potential as functional agents for safeguarding human health against radiation-induced damage.

β-ecdysterone, a functional component derived from medicine and food homologous herb Achyranthes bidentata, has shown potential in cardiovascular protection according to our previous studies. This study aims to further investigate its neuromodulatory mechanism in cardiac hypertrophy. The anti-hypertrophic effects of β-ecdysterone were validated both in vivo and in vitro. Transcriptomic analysis of cardiac and medullary tissues revealed the involvement of neuroregulatory pathways, including modulation of sympathetic acitivity. β-ecdysterone significantly reduced norepinephrine (NE) levels and its metabolites, which correlated with hypertrophic markers. Weighted Gene Co-Expression Network Analysis (WGCNA) identified Dhx37 as a key gene associated with cardiac hypertrophy. In a co-culture model of sympathetic neurons (PC-12) and cardiomyocytes (H9C2), β-ecdysterone suppressed NE secretion and calcium influx in PC-12 cells under Angiotensin II (AngII) stimulation, an effect abolished by .Dhx37 knockdown in cardiomyocytes. These findings suggest that β-ecdysterone alleviates cardiac hypertrophy by modulating cardiac-sympathetic neuron interaction via the Dhx37 pathway, offering a novel neurocardiac regulatory target for MFH-based therapies.

Hypertrophic cardiomyopathy (HCM) and hypertension often coexist, sharing common etiological factors and pathological mechanisms. Both traditional and modern medicine have explored food and medicine products for their treatment This study examines the therapeutic potential and mechanisms of Achyranthis bidentatae radix and Saururus chinensis, two natural products used in food and medicine homology, in addressing HCM and hypertension. Bioinformatics and computer-aided drug design (CADD) approaches were utilized to identify active ingredients and mechanisms. In vivo and ex vivo experiments were performed to validate the pharmacological effects under conditions mimicking HCM and hypertension. Disease-related genes were identified using GeneCards and DisGeNET, while key components were identified via Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). A total of 62 disease-related genes were identified, with 20 significant components for A. bidentatae radix and 5 for S. chinensis Intersection analysis highlighted 18 common target genes involved insulin-like growth factor 1 receptor (IGF1R), insulin receptor (INSR), insulin (INS), Matrix Metallopeptidase 9 (MMP9), signal transducer and activator of transcription 3 (STAT), were confirmed through real-time PCR in vivo. Molecular docking studies demonstrated direct interactions between quercetin and IGF1R, INSR, MMP9, and between inophyllum E and INS. Molecular dynamics simulations showed favorable binding of quercetin with INSR. Quercetin exhibited promising drug-likeness and therapeutic potential in angiotensin II-treated cardiomyocytes. In conclusion, quercetin, identified as active component in A. bidentatae radix and S. chinensis, shows promising therapeutic effects against HCM and hypertension. These findings highlight the potential of these natural products in cardiovascular disease management through targeted molecular interactions. Future research should explore the nature products with long-term effects in comprehensive cardiovascular disease treatment.

Background: Medicine and food homologous (MFH) products provide enhanced safety and tolerability. This study aimed to identify functional MFH compounds against cardiac hypertrophy. Methods: Bioinformatics analysis and in vivo experiments were utilized to pinpoint key genes in cardiac remodeling. A functional component screening was performed using the Medical Homology Compound Database (MHCD), followed by an evaluation of drug-like properities. Pharmacological assessments included measures of cardiac function, cardiac hypertrophy and fibrosis determination, and mitochondrial function. Transcriptome analysis was carried out to explore potential mechanisms. Interaction studies involved luciferase reporter assays, chromatin immunoprecipitation (ChIP) assays, and loss-of- and gain-of-function verifications. Results: NRF2 has been identified as a critical gene in cardiac remodeling. Among the MHCD compounds, β-ecdysterone was the most promising NRF2 enhancer, showing dose-dependent effectiveness in reversing cardiac remodeling. High concentration of β-ecdysterone resulted in approximately a 2.15-fold improvement. Downregulation of NRF2 negated the beneficial effects of β-ecdysterone, increasing cardiac hypertrophy by roughly 2.14-fold, oxidative stress by 1.94-fold, and mitochondrial dysfunction by 1.69- to 2.14-fold. Slc41a3 was identified and confirmed as being directly regulated by NRF2. Under AngII stimulation, knockdown of Slc41a3 in cardiomyocytes reduced mitochondrial oxidative stress by 87.9% and mitochondrial dysfunction by 1.8-fold. Overexpression of Slc41a3 counteracted the protective effects of β-ecdysterone, elevating mitochondrial oxidative stress by approximately 1.75-fold and impairing mitochondrial function by 1.75- to 2.93-fold in cardiomyocytes. Conclusions: β-ecdysterone alleviates cardiac hypertrophy via the NRF2/Slc41a3 pathway, regulating oxidative stress and mitochondrial dysfunction.