[This corrects the article DOI: 10.1016/j.jgr.2024.08.004.].
[This corrects the article DOI: 10.1016/j.jgr.2024.08.004.].
Background: Ginseng Berry Concentrate (GBC) enhances exercise capacity in mice, but the effects of its key component, ginsenoside Re (G-Re), on aging and mitochondrial function are not well understood. This study investigates the impact of G-Re on mitophagy and its potential to promote healthy aging.
Methods: Experiments in C2C12 myocytes and HeLa-mitoKeima-PARKIN cells assessed GBC and G-Re's effects on mitophagy, supported by Gene Set Enrichment Analysis. G-Re was identified as the primary component of GBC via high-performance liquid chromatography. The influence of G-Re on lifespan and healthspan was examined in Caenorhabditis elegans, with a focus on mitophagy pathways.
Results: GBC and G-Re significantly induced mitophagy and enhanced mitochondrial gene expression, improving mitochondrial function. G-Re extended lifespan and healthspan in C. elegans, effects absent in mitophagy-impaired mutants.
Conclusion: G-Re enhances mitochondrial function and promotes healthy aging through mitophagy, suggesting its potential for mitigating age-related functional declines.
Background: Subcritical water (SW) is regarded as an effective conversion technology for lignocellulosic biomass. The effect of SW on ginseng are limited to evaluate the ginsenoside composition of red ginseng, and there is little information on the effects of SW on fresh ginseng.
Methods: The general characteristics of ginseng extracts (GE) prepared with SW were evaluated in terms of brix, reducing sugar and residual solid content, and compositions of GE was estimated using chromatography. For utilization of GE as a bioactive food, the ginsenoside composition, antioxidative activity, angiotensin-converting enzyme (ACE) inhibitory activity, prebiotic potential and taste attributes were measured.
Results: Increasing SW temperature decreased residual solid content of ginseng and the soluble compounds of GE were yielded by SW at 250 °C. Despite that ginsenoside content decreased with SW temperature, a steep increase in Rg5 was observed at 200 °C. The SW at 200-250 °C manifested the highest antioxidant activities and ACE inhibitory activity of GE. However, the GE prepared at greater than 250 °C completely lost prebiotic potentials. Based on electronic-tongue, umami taste was enhanced by SW at 200 °C, but sweetness and bitterness were dominated at 250-300 °C.
Conclusion: The results demonstrated that SW has a potential application to convert lignocellulosic wastes generated from ginseng roots into bioactive food resource, and SW at ∼200 °C can be potentially used to enhance the physiological activities of GE.
Background: Korean Red Ginseng and ginsenosides have been studied for their efficacy against various diseases, including those related to aging. However, most aging studies use D-galactose to induce aging, which often does not accurately represent natural aging. This study aimed to verify improvements in auditory, cognitive, and liver function through administering red ginseng to an 18-month-old naturally aging mouse model.
Methods: Auditory function was assessed using Auditory Brainstem Response (ABR) and Auditory Middle Latency Response (AMLR). Cognitive function was evaluated electrophysiologically with P300 and mismatch negativity (MMN), and behaviorally using the Y-maze. Additionally, biochemical tests and histological analysis were conducted to assess liver function. The effects of red ginseng on gene expression regulation were also examined in the cochlea, auditory cortex, and liver, focusing on age-related disease processes.
Results: Red ginseng significantly decreased hearing thresholds and improved central auditory function. It also enhanced cognitive behavior and function in response to external stimulation. Furthermore, red ginseng regulated alkaline phosphatase (ALP), albumin (Alb), and total protein (TP) levels, notably decreasing aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Hematoxylin and eosin (H&E) staining of liver tissue showed significant improvement in fat droplets. These effects appear to be mediated by the regulation of aging-related genes Dec, c-Jun, Stat5b, and Lims2.
Conclusion: These results suggest that red ginseng improves auditory, cognitive, and liver functions in a naturally aged mouse model.
Background: Vascular endothelial dysfunction (VED) is one of the main pathogenic events in pulmonary arterial hypertension (PAH). Previous studies have demonstrated that the ginsenoside Rg1 (Rg1) can ameliorate PAH, but the mechanism by which Rg1 affects pulmonary VED in hypoxia-induced PAH remains unclear.
Methods: Network pharmacology, molecular docking and other experiments were used to explore the mechanisms by which Rg1 affects PAH. A PAH mouse model was established via hypoxia combined with the vascular endothelial growth factor (VEGFR) inhibitor su5416 (SuHx), and a cell model was established via hypoxia. The functions of Rg1 in VED, oxidative stress, inflammation, mitophagy, and TXNIP and NLRP3 expression were examined.
Results: In hypoxia-induced VED, progressive exacerbation of oxidative stress, inflammation, and mitophagy were observed, and were associated with elevated TXNIP and NLRP3 expression in vivo and in vitro. Rg1 improved hypoxia-induced impaired endothelium-dependent vasodilation and increased nitric oxide (NO) and endothelial NO synthase (eNOS) expression. Rg1, SRI37330 (a TXNIP inhibitor), MCC950 (an NLRP3 inhibitor), and Liensinine (a mitophagy inhibitor) attenuated oxidative stress, inflammation, and mitophagy by reducing the expression of TXNIP and NLRP3 in mice and cells. Furthermore, the combination of SB203580 (a mitophagy agonist) with Rg1 disrupted the protective effect of Rg1 on hypoxia-induced pulmonary artery and human pulmonary artery endothelial cells (HPAECs).
Conclusion: Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through TXNIP/NLRP3 pathway-modulated oxidative stress, inflammation and mitophagy.
Background: The non-saponin (NS) fraction is an important active component of Panax ginseng, with multifunctional pharmacological activities including neuroprotective, immune regulatory, anti-inflammatory, and antioxidant effects. However, the effects of NSs on multiple sclerosis (MS), a chronic and autoimmune demyelinating disorder, have not yet been demonstrated.
Purpose: and Methods: The goal of the present study was to demonstrate the pharmacological actions of NSs on movement dysfunctions and the related mechanisms of action using an experimental autoimmune encephalomyelitis (EAE) mouse model of MS.
Results: NSs (p.o.) alleviated movement dysfunctions in EAE mice related to reduced demyelination in the lumbar spinal cord (LSC). NSs attenuated the recruitment of microglia (CD11b+/CD45low) and macrophages (CD11b+/CD45high) in LSCs from EAE model mice, consistent with the decreased mRNA expression levels of the main proinflammatory mediators (IL-1β, COX-2, MCP-1, MIP-1α, and RANTES). NSs blocked the migration of Th17 cells (CD4+/IL17A+) and mRNA expression levels of IL-17A (product of Th17 cells) in LSCs from EAE mice. NSs suppressed alterations in blood-brain barrier (BBB) components, such as astrocytes and cell adhesion molecules, associated with inhibiting NF-κB and p38 MAPK pathways in LSCs of EAE mice and lipopolysaccharide-induced bEND.3 cells.
Conclusions: NSs could attenuate movement dysfunctions and related pathological/inflammatory changes by reducing BBB permeability through NF-κB and p38 MAPK pathway inhibition in LSCs of EAE model mice. These are the first results suggesting that NSs can be potential therapeutic agents for MS by reducing BBB permeability.