{"title":"Total saponins from Panax notoginseng leaves alleviate complex insomnia by modulating neuroendocrine function, synaptic plasticity, and energy metabolism","authors":"Yu-Peng Liu, Ling-Yun Chou, Wen-Jia Yuan, Bing-Chen Han, Han Cheng, Yue-Bin Ge, Jian-Bo Wan, Xian-Ju Huang","doi":"10.1016/j.jgr.2026.101082","DOIUrl":"10.1016/j.jgr.2026.101082","url":null,"abstract":"<div><h3>Background</h3><div>Insomnia is increasingly recognized as a multifactorial disorder characterized by neuroendocrine imbalance, synaptic dysfunction, and impaired energy metabolism, particularly under conditions of chronic stress. Qiye Shen'an Tablets, formulated from total saponins of <em>Panax notoginseng</em> leaves (PNL), are widely used in clinical practice, however, their active constituents and underlying mechanisms remain incompletely understood. Notably, partial hydrolysis of saponins during the preparation process may modify their chemical composition, thereby potentially influencing therapeutic efficacy.</div></div><div><h3>Methods</h3><div>Total saponins before (TS-b) and after hydrolysis (TS-a), along with a commercial reference preparation (TS-a+b), were comparatively evaluated in a mouse model of insomnia induced by 4-chloro-DL-phenylalanine (PCPA) combined with systemic stress. Behavioral assessments, hematological analysis, neurotransmitter quantification, histological examination, and metabolomic profiling were conducted. In addition, key pathways associated with the hypothalamic–pituitary–adrenal (HPA) axis and synaptic plasticity were investigated. The neuroprotective effect of notoginsenoside Fd, a major component of TS-a, was further examined in glutamate-injured hippocampal neurons.</div></div><div><h3>Results</h3><div>Compared with TS-b and TS-a+b, TS-a exhibited a more stable composition and superior therapeutic efficacy. It significantly improved sleep-related behaviors, alleviated emotional disturbances, and partially normalized hematological parameters and neurotransmitter levels. Mechanistic analyses indicated that TS-a attenuated dysregulation of HPA axis, mitigated hippocampal glucocorticoid receptor (GR) overactivation, and enhanced the PKA–CREB–BDNF pathway, accompanied by increased expression of synaptic proteins. Metabolomic profiling further suggested the involvement of pathways related to neurotransmission and mitochondrial energy metabolism. Notoginsenoside Fd conferred neuroprotection against glutamate-induced neuronal injury, potentiallythrough modulation of GR signaling.</div></div><div><h3>Conclusion</h3><div>TS-a relieves complex insomnia through coordinated regulation of stress response, synaptic function, and energy metabolism, thereby providing scientific basis for optimizing preparation processes and refining active constituents.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 5","pages":"Article 101082"},"PeriodicalIF":7.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148305760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Direct targeting of ORAI1 by ginsenoside Rg3 modulates calcium signaling and senescence-associated AMPK-NRF2 activation","authors":"Sooyeon Lee, Minjeong Ko, Ho Jeong Kwon","doi":"10.1016/j.jgr.2026.101069","DOIUrl":"10.1016/j.jgr.2026.101069","url":null,"abstract":"<div><h3>Background</h3><div>20(S)-ginsenoside Rg3 (Rg3(S)), a major saponin derived from red ginseng, exhibits diverse biological activities, including antioxidant and anti-senescence effects. However, the direct molecular targets through which Rg3(S) regulates calcium signaling and its role at membrane contact sites during cellular senescence remain largely unknown.</div></div><div><h3>Methods</h3><div>Plasma membrane (PM)-endoplasmic reticulum (ER) contacts and related protein interactions were analyzed using proximity ligation assays and co-immunoprecipitation. Direct binding of Rg3(S) to ORAI1 was validated using cellular thermal shift assays and microscale thermophoresis. Molecular docking simulations followed by site-directed mutagenesis were used to define critical binding residues. Cytosolic calcium levels and cellular senescence were assessed using calcium imaging and senescence-associated β-galactosidase staining.</div></div><div><h3>Results</h3><div>Rg3(S) increased cytosolic calcium levels independently of ER calcium depletion and was accompanied by a reduction in PM-ER contacts. Rg3(S) directly bound to ORAI1 in a dose-dependent manner, identifying ORAI1 as a previously unrecognized molecular target of ginsenoside Rg3. Molecular docking revealed LYS204 and ILE229 within the extracellular loop of ORAI1 as key residues maintaining this interaction. Mutation of these residues abolished Rg3(S)-induced calcium influx, leading to impaired activation of the AMPK-NRF2 pathway and attenuation of the anti-senescence effect of Rg3(S).</div></div><div><h3>Conclusion</h3><div>These findings identify ORAI1 as a key molecular mediator of ginsenoside Rg3(S)-induced calcium signaling linked to cellular senescence. By modulating PM-ER contact sites and cytosolic calcium dynamics, Rg3(S) attenuates senescence, providing new mechanistic insight into the anti-aging potential of ginseng-derived compounds beyond autophagy-centered pathways.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 5","pages":"Article 101069"},"PeriodicalIF":7.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148861675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhuoqun Wang, Linxin Zhang, Chang Liu, Shuang Yan, Mengyang Wang
{"title":"Unveiling a novel pathway: Ginseng vanillic acid fights heart failure by coupling mitophagy to pyroptosis through the PINK1-BRCA1-NLRP3 axis","authors":"Zhuoqun Wang, Linxin Zhang, Chang Liu, Shuang Yan, Mengyang Wang","doi":"10.1016/j.jgr.2026.101076","DOIUrl":"10.1016/j.jgr.2026.101076","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure (HF) represents a frequent and serious complication of hypertensive diseases. Substantial evidence has implicated angiotensin II (Ang II) in the promotion of cardiac remodeling and inflammation associated with hypertension. Vanillic acid (VA), an organic acid derived from natural sources such as ginseng, demonstrates a spectrum of bioactivities including anti-inflammatory and antioxidant effects.</div></div><div><h3>Purpose</h3><div>This study aimed to elucidate the potential of VA in attenuating Ang II-induced HF and to delineate its underlying mechanism of action.</div></div><div><h3>Methods</h3><div>In C57BL/6 mice, HF was induced by 4-week Ang II infusion. To delineate the cardioprotective mechanisms of VA, mice were treated with VA orally for 2 weeks following the initial 2 weeks of Ang II exposure, with subsequent cardiac RNA sequencing. VA-binding proteins were validated by molecular docking, DARTS, CETSA, and SPR.</div></div><div><h3>Results</h3><div>VA significantly ameliorated cardiac dysfunction without affecting blood pressure, concurrently suppressing cardiac fibrosis, hypertrophy, and inflammation. RNA sequencing implicated the PINK1 pathway, which was supported by in vitro observations of improved mitochondrial morphology and autophagic flux in NRVMs. Furthermore, direct binding between VA and BRCA1 was confirmed by molecular docking, DARTS, CETSA, and SPR.</div></div><div><h3>Conclusions</h3><div>This study demonstrates that VA suppresses NLRP3 inflammasome-mediated heart failure by restoring cardiomyocyte mitochondrial function through the PINK1- BRCA1 signaling axis. These findings identify VA as a promising therapeutic candidate for HF and support its further development as a novel agent targeting mitophagy and metabolic recovery in the stressed heart.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 5","pages":"Article 101076"},"PeriodicalIF":7.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148859240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thi Hong Ngo, Em Canh Pham, Linh Duy Nguyen, Thanh Thao Vu, Duy Hoang Truong, Ho Phuong Uyen LE, Thi Thu Thao Nguyen, Tuyen Ngoc Truong, Duc Viet Ho, Thi Hong Van LE
{"title":"Novel indole alkaloids from the flower buds of Panax vietnamensis var. fuscidiscus: Distribution in reproductive organs and integrated biological evaluation","authors":"Thi Hong Ngo, Em Canh Pham, Linh Duy Nguyen, Thanh Thao Vu, Duy Hoang Truong, Ho Phuong Uyen LE, Thi Thu Thao Nguyen, Tuyen Ngoc Truong, Duc Viet Ho, Thi Hong Van LE","doi":"10.1016/j.jgr.2026.101106","DOIUrl":"10.1016/j.jgr.2026.101106","url":null,"abstract":"<div><h3>Background</h3><div>While the chemical constituents of flower buds from several <em>Panax</em> species have been reported, the phytochemical profile of the flower buds of Vietnamese ginseng remains understudied, particularly alkaloids. This study aimed to characterize alkaloids from the flower buds of <em>Panax vietnamensis</em> var. <em>fuscidiscus</em> (PVF), investigate their distribution across reproductive plant parts, and their biological relevance.</div></div><div><h3>Methods</h3><div>Flower buds were extracted with methanol, then fractionated by liquid–liquid partitioning and chromatography. Structures of isolated compounds were elucidated using NMR and MS. Their distribution in flower buds and various berry stages was analysed by HPTLC, HPLC/PDA, and UPLC-QToF-MS. Anti-bacterial activity was evaluated <em>in vitro</em>, and molecular docking with <em>in silico</em> ADMET analysis was conducted to explore potential targets and pharmacokinetic characteristics.</div></div><div><h3>Results</h3><div>Two novel indole alkaloids, panaxindolic acid and pyrindolic acid, with the known alkaloid panaxindole and tryptophan, were isolated. All identified alkaloids were detected in multiple reproductive parts, indicating a broad distribution. Docking simulations predicted strong binding of the isolated alkaloids toward monoamine oxidase B (MAO-B) through hydrogen bonding and π-π stacking with key residues, including CYS172 and TYR398. Although panaxindole exhibited limited anti-bacterial activity <em>in vitro</em>, computational analyses suggested potential interactions with bacterial DNA gyrase and the 30S ribosomal subunit. ADMET predictions indicated favorable pharmacokinetic profiles and low toxicity.</div></div><div><h3>Conclusion</h3><div>This study presents the first systematic investigation of indole alkaloids from PVF flower buds and their distribution across reproductive organs. Although <em>in vitro</em> anti-bacterial activity of panaxindole was limited, <em>in silico</em> analyses highlight potential biological relevance to neurodegenerative disease-associated targets.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 5","pages":"Article 101106"},"PeriodicalIF":7.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148859657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Total saponins from Panax ginseng delay aging and cellular senescence via PI3K-AKT pathway in a rapid dual-system screening model of aging","authors":"Yu-jing Tan, Wen-qi Jin, Jing Wang, Hui Wang, Ting-ting Lou, Li-wei Sun, Fang-bing Liu, Shuai Zhang","doi":"10.1016/j.jgr.2026.101105","DOIUrl":"10.1016/j.jgr.2026.101105","url":null,"abstract":"<div><h3>Background</h3><div>Aging, as an inevitable biological process, is an inevitable process of multisystem functional decline, with cellular senescence being one of its hallmarks. Although total saponins from <em>Panax ginseng</em> (TSG) offer health benefits, its precise anti-aging mechanisms have not been fully elucidated.</div></div><div><h3>Methods</h3><div>A rapid dual-system screening model of aging was established using tert-butyl hydrogen peroxide (tBHP) to induce senescence in human umbilical vein endothelial cells (HUVECs) and <em>Caenorhabditis elegans</em> (<em>C. elegans</em>). Anti-aging effects and key components of TSG were evaluated <em>via</em> fluorescent staining, Western blotting (WB), and biochemical and behavioral analysis. Bioinformatics analysis, WB, AKT activator and loss-of-function mutants in <em>C. elegans</em> were used to clarify TSG's anti-aging and anti-cellular senescence effects <em>via</em> PI3K-AKT signaling.</div></div><div><h3>Results</h3><div>TSG alleviated oxidative stress, enhanced antioxidant capacity and reduced β-galactosidase activity, indicating delayed aging. It also modulated senescence-related markers and increased Ki-67, supporting its role in promoting proliferation and suppressing cellular senescence. Among 20 ginsenosides screened, PPD, F1 and Rh1 were identified as the principal active components. Network pharmacology and experimental validation revealed the PI3K-AKT pathway as central to TSG's effects. AKT1 and PI3K were confirmed as the targets, with decreased phosphorylation levels observed. TSG's anti-aging effects were partly abolished in loss-of-function mutant worms <em>akt-1;akt-2</em> and <em>age-1</em>, substantiating the essential role of PI3K-AKT signaling <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>This study establishes a rapid dual-system model for aging research, and demonstrates that TSG and its principal ginsenosides (PPD, F1 and Rh1) mitigate aging and cellular senescence through the PI3K-AKT pathway by downregulating PI3K/AKT phosphorylation.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 5","pages":"Article 101105"},"PeriodicalIF":7.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ginsenoside Rh2, a putative functional modulator of Annexin A2, attenuates post-hemorrhagic stroke cerebral edema via inhibiting vesicular transcytosis","authors":"Xu Han, Chu Li, Qianlin Li, Haixia You, Feiyan Chen, Cuihua Chen, Qi Yao, Dongqing Yang, Lin Chen, Zhu Zhu, Yunan Zhao","doi":"10.1016/j.jgr.2026.101148","DOIUrl":"https://doi.org/10.1016/j.jgr.2026.101148","url":null,"abstract":"Background Intracerebral hemorrhage (ICH) causes mechanical damage and cerebral edema. Annexin A2, expressed in endothelial cells, regulates cerebral edema, but its mechanisms in ICH remain unclear. Methods A mouse ICH model was established using collagenase VII-S. We measured Annexin A2 expression, transcytosis, and blood–brain barrier (BBB) permeability. AAV was used to specifically knock down Annexin A2 in cerebrovascular endothelial cells. Protein interactions were identified by co-immunoprecipitation and label-free LC-MS. Ginsenoside Rh2 was tested for effects on protein binding (biolayer interferometry and competition assays) and on neurological/motor function, BBB integrity, and transcytosis. Results ICH increased Annexin A2 expression, transcytosis, and BBB permeability. Annexin A2 knockdown worsened neurological deficits and motor function, increased BBB permeability, exacerbated tight junction disruption, but significantly reduced transcytosis. Six cytoskeletal proteins, Alpha-actinin-4, Actin-related protein 2, Actin alpha skeletal muscle, Actin cytoplasmic 1, Actin cytoplasmic 2, and Myosin-9, interacted with Annexin A2. Rh2 reduced binding affinity between Annexin A2 and these proteins, specifically inhibiting Annexin A2–Alpha-actinin-4 binding. Rh2 treatment improved neurological and motor function, reversed BBB disruption and tight junction damage, and suppressed transcytosis without altering Annexin A2 expression. Conclusion Annexin A2 knockdown inhibited transcytosis but disrupted tight junctions and aggravated edema. In contrast, Rh2 inhibited transcytosis and exerts potential protective effect tight junctions, which may suggest a trend toward alleviation of cerebral edema to a certain extent. Selectively targeting Annexin A2-mediated transcytosis may be a promising therapy for ICH.","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"1 1","pages":"101148-101148"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148861169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ginsenosides: potential therapeutic agents against hepatic fibrosis","authors":"Zhengzheng Wu, Yi Liu","doi":"10.1016/j.jgr.2026.101055","DOIUrl":"10.1016/j.jgr.2026.101055","url":null,"abstract":"<div><div>Hepatic fibrosis, for which no effective pharmacological interventions currently exist, is characterized by progressive scarring and architectural distortion. The pathogenesis involves excessive accumulation of extracellular matrix components, predominantly synthesized by activated hepatic stellate cells (HSCs). HSCs can be activated by inflammatory signals and injured hepatocytes, processes linked to intestinal microbiota dysbiosis. Therefore, HSCs and associated pathways constitute promising therapeutic targets for antifibrotic strategies. Recent evidence suggests that ginsenosides, principal bioactive constituents of <em>Panax ginseng,</em> demonstrate hepatoprotective and antifibrotic properties. Ginsenosides are structurally classified into dammarane-type, ocotillol-type, and oleanane-type saponins, showing favorable safety profiles. Their pharmacological activity is critically dependent on structural features, including the quantity, type, and glycosylation positions of sugar moieties, as well as the stereochemical configuration at the C-20 position. The antifibrotic mechanisms of ginsenosides encompass multiple pathways: suppression of HSC activation, induction of HSC death, amelioration of hepatocellular injury, attenuation of inflammatory responses, and modulation of intestinal microbiota composition. This review aims to evaluate ginsenosides as potential therapeutic agents for hepatic fibrosis and to establish a theoretical framework for their clinical translation in the management of this condition.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101055"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13324066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Woo Kyu Kang, Sun-Young Hwang, Hyunjin Kang, Jin Won Hyun, Sang-Kyu Kim, Mee-Hyun Lee
{"title":"Microbiome-mediated pharmacology of ginseng: Mechanistic insights into metabolic regulation and therapeutic potential","authors":"Woo Kyu Kang, Sun-Young Hwang, Hyunjin Kang, Jin Won Hyun, Sang-Kyu Kim, Mee-Hyun Lee","doi":"10.1016/j.jgr.2026.101023","DOIUrl":"10.1016/j.jgr.2026.101023","url":null,"abstract":"<div><div>Ginseng, a traditional medicinal herb with a favorable safety profile, has long been used to promote systemic health. Recent studies reveal that many of its beneficial effects are mediated through interactions with the gut microbiota. Microbial enzymes convert parent ginsenosides into more absorbable and bioactive metabolites such as compound K, while ginseng reciprocally remodels the microbial community and metabolite composition by promoting the growth of beneficial taxa including <em>Akkermansia</em>, <em>Bifidobacterium</em>, and <em>Lactobacillus</em>. These bidirectional interactions modulate host metabolic, immune, and intestinal barrier functions. The ginseng–microbiome interplay regulates microbial and host-derived metabolites such as short-chain fatty acids, bile acids, and indole derivatives, which in turn activate key signaling pathways including FXR/TGR5, FFAR, AMPK, and Nrf2. Through these mechanisms, ginseng improves lipid metabolism, enhances insulin sensitivity, alleviates low-grade inflammation, and ameliorates metabolic abnormalities such as obesity, insulin resistance, and nonalcoholic fatty liver disease (NAFLD). This review provides a comprehensive synthesis of the ginseng–microbiota metabolic axis, focusing on its mechanistic basis in metabolic regulation and related disorders. We also highlight the therapeutic convergence between ginseng and probiotics possessing ginsenoside-hydrolyzing enzymes, discuss strategies for strain selection and co-administration, and outline future directions in precision, microbiome-informed formulations and clinical trial design. Collectively, current evidence supports the ginseng–microbiota interactions as a promising therapeutic platform for restoring metabolic homeostasis and managing metabolic diseases.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101023"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dong Hyun Lee, Chul Hee Lee, Tae Young Kim, Junwon Lee, Eun Young Choi, Min Kim
{"title":"Effect of Korean red ginseng on deep capillary plexus parameters in diabetic retinopathy: A prospective, randomized, double-blind clinical trial","authors":"Dong Hyun Lee, Chul Hee Lee, Tae Young Kim, Junwon Lee, Eun Young Choi, Min Kim","doi":"10.1016/j.jgr.2026.101025","DOIUrl":"10.1016/j.jgr.2026.101025","url":null,"abstract":"<div><h3>Background</h3><div>This prospective, randomized, double-blind clinical trial aimed to evaluate the effects of Korean Red Ginseng (KRG) extract on the retinal microvascular parameters in patients with diabetic retinopathy (DR).</div></div><div><h3>Methods</h3><div>Patients with mild to moderate non-proliferative DR were randomized to receive KRG extract or placebo for 90 days. Outcomes included changes in the best-corrected visual acuity (BCVA), intraocular pressure (IOP), central macular thickness (CMT), and optical coherence tomography angiography (OCTA) parameters, including the foveal avascular zone, vessel length density (VLD), and perfusion index (PI) in the superficial and deep capillary plexuses (SCP and DCP, respectively). The incidence of proliferative DR or diabetic macular edema (DME) was also monitored.</div></div><div><h3>Results</h3><div>Twenty-four patients were enrolled and 23 completed the study. The baseline BCVA, IOP, CMT, and OCTA parameters were comparable between the groups (all p > 0.05). No significant changes were observed in BCVA, CMT, DR severity stage, or incidence of DME over the 3-month follow-up period in either group. Significant group × time interaction effects were observed for inferior DCP VLD (p = 0.011) and for PI in the superior (p = 0.044) and inferior (p = 0.026) DCP regions. No significant interaction effects were identified for SCP parameters or other DCP subfields. No adverse events were reported.</div></div><div><h3>Conclusions</h3><div>KRG extract was associated with short-term, region-specific changes in OCTA-derived DCP perfusion metrics over 3 months. These findings reflect alterations in OCTA-derived microvascular parameters and do not establish modification of clinical outcomes such as DR progression or the development of DME.</div></div><div><h3>Trial registration</h3><div>Clinical Research Information Service, #KCT0010991.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101025"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ji-Hun Kim, Rami Lee, Sung-Hee Hwang, Yebeen Kang, Hyun-Mee Park, Sun-Hye Choi, BaiCheng Chen, Jong-Hoon Kim, Seung-Yeol Nah
{"title":"Neo-gintonin: production of high concentrations of lysophosphatidic acids from Korean Red ginseng marc","authors":"Ji-Hun Kim, Rami Lee, Sung-Hee Hwang, Yebeen Kang, Hyun-Mee Park, Sun-Hye Choi, BaiCheng Chen, Jong-Hoon Kim, Seung-Yeol Nah","doi":"10.1016/j.jgr.2026.101060","DOIUrl":"10.1016/j.jgr.2026.101060","url":null,"abstract":"<div><h3>Background</h3><div>Gintonin is a novel non-saponin glycolipoprotein complex that is derived from ginseng. Its functional components are lysophosphatidic acids (LPAs), which act as ligands for six G protein-coupled LPA receptor subtypes. Thus, gintonin exerts it activity through the LPA receptor signaling pathway. Previous studies have shown that crude gintonin derived from Korean Red ginseng marc (KRGM) contains approximately 0.2–0.3% LPAs. The aim of this study was to develop a method for concentrating the LPA content in KRGM-derived gintonin.</div></div><div><h3>Methods</h3><div>First, we prepared a gintonin-enriched fraction from KRGM and removed its ethanol-insoluble portion. Then, the ethanol-soluble fraction was subjected to anion-exchange chromatography followed by gel filtration. Subsequently, the gintonin fractions were collected and freeze-dried. The presence of the glycolipoprotein complex was confirmed using SDS-PAGE and gel staining. The newly acquired product was designated neo-gintonin.</div></div><div><h3>Results</h3><div>Compared with KRGM total extract, neo-gintonin contained 15.4-fold higher concentrations of LPA C18:2, LPA C16:0, and LPA C18:1. The approximately 66 kDa neo-gintonin was H<sub>2</sub>O highly water soluble. In primary cortical astrocytes treated with fluorescent neo-gintonin (prepared using Alexa Fluor 488 NHS ester), the fluorescent complex was found to bind to the cell membrane. This binding could be blocked using an LPA1/3 receptor antagonist. Neo-gintonin also stimulated nerve growth factor release from mouse primary cortical astrocytes.</div></div><div><h3>Conclusion</h3><div>We developed a novel method for extracting neo-gintonin from KRGM and demonstrated that it exerted its physiological effects via LPA receptors. Thus, KRGM is a novel gintonin source and can be upcycled to prepare high LPA-yielding neo-gintonin.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101060"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}