Journal of Ginseng Research最新文献

{"title":"Ginsenosides from Panax ginseng: Their mechanisms, microbiome determinants, and translational strategies in therapeutic activity against cancer","authors":"Canglang Mou,&nbsp;Yuhao Wang,&nbsp;Mi-Yeon Kim,&nbsp;Jae Youl Cho","doi":"10.1016/j.jgr.2026.101029","DOIUrl":"10.1016/j.jgr.2026.101029","url":null,"abstract":"<div><div>Ginsenosides from <em>Panax ginseng</em> Meyer and their microbiota-derived metabolites have been explored as adjuncts in oncology, with pleiotropic activities across tumor-intrinsic and microenvironmental pathways. This review focuses on representative metabolites (Rg3, Rh2 and compound K) and summarizes mechanistic evidence for apoptosis and cell-cycle control, metabolic reprogramming (Warburg-type glycolysis), and epigenetic regulation (miRNA/lncRNA-linked programs), together with immunomodulatory effects in the tumor microenvironment. A central translational constraint is pharmacokinetics and the “microbiota gatekeeping” effect: many parent ginsenosides show limited oral absorption and require microbiota-mediated deglycosylation, resulting in delayed and variable systemic exposure across individuals. To address this bottleneck, we discuss pragmatic translational directions including bioconversion/pre-transformation to enrich active metabolites, biomimetic delivery platforms such as ginseng-derived exosome-like nanoparticles to improve exposure and tissue uptake, and mechanism-guided combinations (e.g., with immune checkpoint blockade). Finally, we outline how biomarker-informed stratification and AI/ML-enabled, hypothesis-generating optimization of delivery/formulation may support more predictable clinical development.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101029"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376026","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":"Li-ginseng powder alleviates cancer cachexia in mice by regulating the ubiquitin-proteasome pathway and reducing inflammation","authors":"Xinghui Jin,&nbsp;Wenyuan Liu,&nbsp;Gang-Ao Li,&nbsp;Ya-Ni Wang,&nbsp;Kwang-Il To,&nbsp;Yang Li,&nbsp;Ying-Hua Jin","doi":"10.1016/j.jgr.2026.101061","DOIUrl":"10.1016/j.jgr.2026.101061","url":null,"abstract":"<div><h3>Background</h3><div>As a debilitating syndrome, cancer cachexia (CC) manifests as ongoing weight reduction and skeletal muscle atrophy, which severely compromise patients’ well-being and life expectancy, with no approved treatment available to date. Rare ginsenosides such as Rh2, Rg5, Rk1, and Rh4 have been reported to modulate Nuclear factor kappa-B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) activity and attenuate inflammatory signaling pathways implicated in CC progression. Li-Ginseng powder (LGP), a specially processed <em>Panax ginseng</em> enriched in rare ginsenosides, including Rk1, Rk3, Rh4, Rg3, and Rg5 represents a potential therapeutic candidate for CC.</div></div><div><h3>Methods</h3><div>The anti-cachexia effects of LGP were evaluated in a BALB/c mouse model of CC and in a cellular CC model using mouse myoblast C2C12 cells. Body weight, skeletal muscle atrophy, and histopathological analyses were performed to assess <em>in vivo</em> efficacy. Network pharmacology was applied to predict key regulatory pathways, and mechanistic validation was conducted using Western blotting, immunohistochemistry, and Enzyme-linked immunosorbent assay.</div></div><div><h3>Results</h3><div>LGP treatment significantly attenuated body weight loss and skeletal muscle atrophy in CC mice. Mechanistically, LGP suppressed activation of the ubiquitin-proteasome pathway in the gastrocnemius muscle and reduced systemic and local inflammatory responses. Network pharmacology analysis identified NF-κB and STAT3 signaling as major targets of LGP, which was further confirmed in both muscle tissues and C2C12 cells. Consistently, LGP alleviated myotube atrophy and inhibited UPP, NF-κB, and STAT3 activation in vitro.</div></div><div><h3>Conclusion</h3><div>These findings demonstrate that LGP exerts protective effects against CC by modulating muscle proteolysis and inflammation-related signaling pathways, highlighting its potential as a ginseng-based therapeutic strategy for CC.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101061"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375989","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":"Efficacy and safety of Korean red ginseng as adjunctive therapy in type 2 diabetes mellitus: a 12-week randomized, double-blind, placebo-controlled trial","authors":"Ji Sun Nam,&nbsp;Jeong Gyu Kim,&nbsp;Chul Woo Ahn,&nbsp;YuSik Kim","doi":"10.1016/j.jgr.2026.101068","DOIUrl":"10.1016/j.jgr.2026.101068","url":null,"abstract":"<div><h3>Background</h3><div>Korean Red Ginseng (KRG) has been investigated as adjunctive therapy for type 2 diabetes mellitus (T2DM), but randomized controlled evidence evaluating metabolic efficacy and short-term safety in patients receiving stable oral antidiabetic therapy remains limited.</div></div><div><h3>Methods</h3><div>In this 12-week randomized, double-blind, placebo-controlled trial, 70 adults with well-controlled T2DM receiving stable oral antidiabetic medications were assigned to KRG (2 g/day) or placebo. Outcomes included oral glucose tolerance test (OGTT)-derived insulin, C-peptide, and glucagon responses, insulin sensitivity indices, fasting plasma glucose (FPG), HbA_1c, oxidative stress markers, antioxidant capacity, lipid profiles, and renal and hepatic safety parameters. Between-group comparisons used baseline-adjusted ANCOVA with Benjamini–Hochberg false discovery rate correction; efficacy analyses included participants with post-baseline data (n = 65).</div></div><div><h3>Results</h3><div>Compared with placebo, KRG was associated with lower 120-min OGTT insulin (adjusted mean difference −6.992, 95% CI −14.205 to −0.222; p = 0.047) and higher ISI(0–120) (5.400, 0.972 to 9.829; p = 0.018). KRG was also associated with lower oxidized low-density lipoprotein (−5.645, −10.054 to −1.238; p = 0.013), malondialdehyde (−0.571, −1.090 to −0.053; p = 0.031), total cholesterol (−12.633, −24.752 to −0.515; p = 0.041), and low-density lipoprotein cholesterol (−10.171, −18.130 to −2.211; p = 0.013). FPG, 2-h glucose, and HbA1c did not differ significantly between groups. No hypoglycemic events occurred, and renal and hepatic safety markers remained stable.</div></div><div><h3>Conclusions</h3><div>KRG was well tolerated and associated with favorable effects on selected indices of postprandial insulin sensitivity, lipid peroxidation markers, and lipid profile in this well-controlled T2DM population. Its short-term metabolic effects may be more apparent in post-load insulin dynamics than in conventional glycemic markers.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101068"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375923","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 Rb1 mitigates senescence-associated hepatic steatosis in mice through enhanced lysine degradation","authors":"Lin Wu,&nbsp;Qi Si,&nbsp;Bin Zhou,&nbsp;Yanyun Che,&nbsp;Yong Liu,&nbsp;Yingying Zhao,&nbsp;Ximei Zhang,&nbsp;Guangyao Shi,&nbsp;Baoshun Hao,&nbsp;Shujie Yu,&nbsp;Xiaoxian Qian,&nbsp;Jianrui Zheng,&nbsp;Dinghui Liu","doi":"10.1016/j.jgr.2026.101026","DOIUrl":"10.1016/j.jgr.2026.101026","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;The liver is the central organ for metabolism and detoxification, and its function gradually declines with age, often accompanied by pathological changes such as lipid metabolism disorders, inflammatory responses, and fibrosis, significantly increasing the risk of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH). Ginsenoside Rb1 (Rb1) is a major active constituent of ginseng. However, its regulatory mechanism on hepatic lipid metabolism and MASLD/MASH-related phenotypes during natural aging remains unclear.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;To explore the effects of Rb1 on liver aging phenotypes, lipid deposition, inflammation, fibrosis, and related metabolic pathways in naturally aged mice, and to further elucidate the underlying regulatory mechanisms.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Naturally aged male C57BL/6J mice (72-week-old) were used and divided into the Old group and the Rb1 treatment group (Old + Rb1). Young mice (6-week-old) served as controls. Therapeutic effects were evaluated through histopathology (H&amp;E, Masson trichrome, Oil Red O staining), immunofluorescence (p21, FASN, FABP1, PPARα), immunohistochemistry (PCNA, F4/80), RT-qPCR analysis of lipid metabolism-related genes. Additionally, untargeted metabolomics analyses of both serum and liver tissues, as well as liver transcriptome sequencing, were performed to investigate the underlying mechanisms.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Rb1 alleviated hepatocellular senescence, as evidenced by reduced p21 expression and increased PCNA-positive cells. It ameliorated age-related hepatic pathological damage, as evidenced by reduced inflammatory infiltration (F4/80) and collagen deposition (Masson staining), along with improved hepatocellular vacuolation and lipid accumulation (Oil Red O staining). Rb1 regulated hepatic lipid metabolism through three mechanisms: inhibiting lipid synthesis (&lt;em&gt;Fasn, Acaca&lt;/em&gt;, &lt;em&gt;Srebf1&lt;/em&gt;), modulating lipid transport (&lt;em&gt;Fabp1&lt;/em&gt;, &lt;em&gt;Slc27a2&lt;/em&gt;), and promoting lipid oxidation (&lt;em&gt;Pparα&lt;/em&gt;, &lt;em&gt;Fgf21&lt;/em&gt;). Serum and hepatic metabolomics consistently revealed that Rb1 activated the lysine degradation pathway, accompanied by an increase in the key intermediate metabolite trimethyllysine (TML). Liver transcriptome sequencing further indicated an increasing trend in the numbers of genes associated with the biological process of metabolic process and the molecular functions of transporter activity and transcription regulator activity. Additionally, enrichment of the biological process of lipid export from the cell was observed in the comparison between the Old and Old+Rb1 groups.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Rb1 ameliorates age-related hepatic lipid accumulation and pathological damage in naturally aged mice by promoting the lysine degradation pathway and comprehensively remodeling lipid metabolic homeostasis. These ","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101026"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375945","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 Rh7 ameliorates myocardial injury in diabetic cardiomyopathy by promoting M2 polarization of macrophages via SIRT1/FOXO1/β-catenin","authors":"Chenyang Han,&nbsp;Shasha wu,&nbsp;Li Zha,&nbsp;Li Guo","doi":"10.1016/j.jgr.2026.101065","DOIUrl":"10.1016/j.jgr.2026.101065","url":null,"abstract":"<div><h3>Aim</h3><div>To investigate the intervention effect of ginsenoside Rh7 on myocardial dysfunction in diabetic cardiomyopathy.</div></div><div><h3>Methods</h3><div>A diabetic cardiomyopathy (DCM) mouse model was established using a high-fat diet combined with streptozotocin (STZ), and treated with ginsenoside Rh7. Echocardiography was used to detect changes in cardiac function in mice. Mouse body weight, heart weight, and cardiac index were measured. H&amp;E staining was used to detect pathological changes in the heart. Tissue chemistry and fluorescence staining were used to detect the expression of CD206 and SIRT1 in the heart. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of M1/M2 cell markers.</div></div><div><h3>Results</h3><div>Rh7 can improve cardiac dysfunction in DCM mice by inhibiting the expression of SIRT1, thereby promoting the activation of the FOXO1/β-catenin complex and M2 polarization of macrophages.In vitro iBMDM experiments showed that Rh7 can promote CD206 expression and M2 polarization of macrophages. Small molecule-protein docking and pull-down experiments confirmed the binding relationship between Rh7 and SIRT1.</div></div><div><h3>Conclusion</h3><div>Rh7 can ameliorate myocardial injury in DCM mice by inhibiting SIRT1 and activating FOXO1/β-catenin, thereby promoting M2 polarization of macrophages.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 4","pages":"Article 101065"},"PeriodicalIF":7.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375998","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":"The cardioprotective mechanism of total saponins from mountain cultivated ginseng against doxorubicin-induced heart failure: Insights from gut-heart axis modulation based on gut microbiota and fecal metabolomics","authors":"Hao Liu ,&nbsp;Ruiqi Zhang ,&nbsp;Zhixuan Mao ,&nbsp;Haiqiang Zhang ,&nbsp;Jincai Lu","doi":"10.1016/j.jgr.2026.100983","DOIUrl":"10.1016/j.jgr.2026.100983","url":null,"abstract":"<div><h3>Background</h3><div>Mountain cultivated ginseng (MCG) has been reported to exert superior therapeutic efficacy in heart failure (HF) models, but the mechanism of total saponins from MCG (TSMCG) remains unclear.</div></div><div><h3>Methods</h3><div>This study aimed to elucidate the mechanism of TSMCG protects against doxorubicin-induced HF through the gut-heart axis. The phytochemical profile of TSMCG was identified using UPLC/Q-TOF-MS. TSMCG (50 or 200 mg/kg) was administered to mice daily for one week before and after doxorubicin exposure. Cardiac function was evaluated via echocardiography, followed by blood biochemical and cardiac histological analyses. Metabolic profiles and gut microbiota composition were analyzed. Fecal microbiota transplantation experiments were employed for mechanistic validation.</div></div><div><h3>Results</h3><div>TSMCG treatment significantly improved cardiac function in HF mice, as evidenced by increased ejection fraction. TSMCG markedly attenuated doxorubicin-induced myocardial injury (CK-MB, NT-proBNP, AST, LDH), oxidative stress (SOD, MDA, CAT, GSH), and cardiac fibrosis. TSMCG effectively regulated key metabolic pathways, particularly tryptophan and bile acid metabolism, and alleviated gut microbiota dysbiosis, particularly <em>Parasutterella</em> and <em>Akkermansia</em>, in HF mice. Close associations between differential microbiota and metabolites were observed. The cardioprotective effects of TSMCG were associated with fecal microbiota transplantation.</div></div><div><h3>Conclusion</h3><div>These findings elucidated the gut-heart axis-based mechanism by which TSMCG alleviated doxorubicin-induced HF and highlighted its potential as a candidate for HF intervention.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 3","pages":"Article 100983"},"PeriodicalIF":5.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147807298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Korean Red ginseng on the regulation of inflammation, cell death, and fibrosis in a mouse model of rheumatoid arthritis featuring spike protein overexpression","authors":"JooYeon Jhun ,&nbsp;Young Joon Lee ,&nbsp;Hyun-Sik Na ,&nbsp;Seung Yoon Lee ,&nbsp;Yeon Su Lee ,&nbsp;Se Gyeong Han ,&nbsp;JeongWon Choi ,&nbsp;Mi-La Cho","doi":"10.1016/j.jgr.2026.101019","DOIUrl":"10.1016/j.jgr.2026.101019","url":null,"abstract":"<div><h3>Background</h3><div>COVID-19 causes inflammation, autoantibody production, and thrombosis-features commonly observed in autoimmune diseases like rheumatoid arthritis (RA). In RA patients infected with COVID-19, immunosuppressive treatments can weaken viral defenses and worsen inflammation. The effects of red ginseng on these patients remain unexplored. We investigated the therapeutic potential of red ginseng extract (RGE) in an RA model with SARS-CoV-2 spike protein overexpression.</div></div><div><h3>Materials and methods</h3><div>Plasmids expressing the SARS-CoV-2 spike protein and ACE2 were delivered into mice with collagen-induced arthritis (CIA). They were orally administered RGE, and effects were assessed via immunohistochemistry, confocal analysis, and ELISA. We analyzed the regulation of Th17 and Treg cells and related cytokines, as well as markers of inflammation, cell death, and fibrosis in splenocytes and fibroblasts. We also examined the combined effects of RGE and methotrexate (MTX).</div></div><div><h3>Results</h3><div>Oral RGE supplementation improved joint inflammation and damage, increasing Treg cells in the spleen. RGE reduced the expression of inflammatory cytokines (IL-17, IL-6, MCP-1, IL-1β, TNF-α), cell death markers (pMLKL, Caspase1), and fibrosis markers (α-SMA, Col1A1) in synovial tissue. In vitro, RGE decreased the expression of these markers in fibroblasts and splenocytes. RGE and MTX had inhibitory effects in the CIA model, with regulatory effects on immune cells, suppressing Th17 cells and enhancing Treg cells.</div></div><div><h3>Conclusion</h3><div>RGE inhibits inflammatory cell death, fibrosis, and modulates immune cells. Its inhibitory effect with MTX suggests therapeutic benefits for RA patients co-infected with COVID-19.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 3","pages":"Article 101019"},"PeriodicalIF":5.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147807300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protopanaxatriol enhances mucin expression in intestinal epithelial cells and mice","authors":"Yeye Hu ,&nbsp;Ziliang He ,&nbsp;Weijie Dai ,&nbsp;Xuejunlan Hu ,&nbsp;Haiyue Hu ,&nbsp;Yuhao Wang ,&nbsp;Lei Huang ,&nbsp;Canglang Mou ,&nbsp;Jinghan Su ,&nbsp;Weizhaole Wei ,&nbsp;Haifeng Wu ,&nbsp;Long You ,&nbsp;Honggang Wang ,&nbsp;Jae Youl Cho ,&nbsp;Weicheng Hu","doi":"10.1016/j.jgr.2026.100992","DOIUrl":"10.1016/j.jgr.2026.100992","url":null,"abstract":"<div><h3>Background</h3><div>Mucins are critical components of the intestinal mucus layer that protects the gut epithelium and maintains microbiota balance. Protopanaxatriol (PPT), an active metabolite derived from protopanaxatriol-type saponins, has shown promise in modulating gut health, but its effects on mucin expression remain poorly understood.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the effects of PPT on mucin expression in human intestinal epithelial Caco-2 cells and in a mouse model.</div></div><div><h3>Methods</h3><div>Caco-2 cells were treated with different concentrations of PPT, and the expression of mucins was assessed via qRT-PCR and Western blot analysis. In parallel, mice were administered PPT orally, and tissues were collected for mucin quantification.</div></div><div><h3>Results</h3><div>PPT treatment significantly upregulated mucin expression at both the mRNA and protein levels in Caco-2 cells. <em>In vivo</em>, mice administered with PPT exhibited significantly elevated mucin expression in the colon. In addition, PPT administration also induced mucin expression in both lung and stomach tissues.</div></div><div><h3>Conclusion</h3><div>PPT promoted mucin expression in human intestinal epithelial cells and in the gut of mice, suggesting their potential as natural agents for maintaining gut health and preventing intestinal disorders.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 3","pages":"Article 100992"},"PeriodicalIF":5.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147807305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Red ginseng-derived components attenuate UVB-induced keratinocyte senescence via senomorphic mechanisms","authors":"Sung Ha Lim,&nbsp;Hee-Seok Seo,&nbsp;Hyun Kang,&nbsp;Seung-Phil Hong","doi":"10.1016/j.jgr.2026.101018","DOIUrl":"10.1016/j.jgr.2026.101018","url":null,"abstract":"<div><h3>Background</h3><div>Senescent cells progressively accumulate within tissues and induce further senescence in neighboring cells through the senescence-associated secretory phenotype (SASP), thereby contributing to tissue dysfunction and aging. While senolytics selectively eliminate senescent cells, senomorphics modulate SASP without inducing cell death. Although red ginseng has been studied for anti-photoaging properties, its role in directly modulating SASP-driven keratinocyte senescence and paracrine aging signaling remains insufficiently defined. This study aimed to investigate whether Korean red ginseng-derived components (RGCs) exert senolytic or senomorphic activity in ultraviolet B (UVB)-induced senescent primary human keratinocytes.</div></div><div><h3>Methods</h3><div>Cellular senescence was induced by repeated UVB irradiation in primary human keratinocytes. A transwell co-culture system was employed to evaluate SASP-mediated paracrine effects on neighboring keratinocytes. Three RGC fractions were examined. Senescence markers (p16 and p21), SASP factors (IL-6, IL-8, IL-1β, and TNF-α), and differentiation/proliferation markers were analyzed. Representative major ginsenosides (Rb1, Rg1, Rg3, Rc) and stress signaling pathways (MAPK/JNK and AKT) were also evaluated.</div></div><div><h3>Results</h3><div>RGCs did not exhibit significant senolytic activity or apoptosis induction. Instead, they demonstrated pronounced senomorphic effects by attenuating UVB-induced upregulation of p16, p21, IL-6, IL-8, and IL-1β. RGCs enhanced keratinocyte proliferation and partially restored early-to-intermediate differentiation markers. In the co-culture model, RGCs mitigated SASP-mediated paracrine effects, reducing senescence and inflammatory signaling in adjacent keratinocytes. These effects were associated with modulation of stress-responsive MAPK/JNK pathways and were partially recapitulated by ginsenosides.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that RGCs function predominantly as senomorphic modulators in UVB-induced keratinocyte senescence, attenuating SASP propagation and stress signaling without inducing cell death.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 3","pages":"Article 101018"},"PeriodicalIF":5.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147807299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rg5 alleviates allergic rhinitis in rats by modulating nasal microbiota by inhibiting JAK2/STAT3/BCL-2 and MAPK signaling","authors":"Chen Bai ,&nbsp;Yue Zhang ,&nbsp;Xiaohui Huo ,&nbsp;Huifang Liu ,&nbsp;Jiyue Sha ,&nbsp;Yinshi Sun ,&nbsp;Jianbo Chen","doi":"10.1016/j.jgr.2026.100984","DOIUrl":"10.1016/j.jgr.2026.100984","url":null,"abstract":"<div><h3>Background</h3><div>Allergic rhinitis (AR) is a non infectious chronic inflammatory disease of nasal mucosa mediated by IgE and driven by type 2 immune response. Ginsenoside Rg5 (Rg5) is a bioactive compound derived from ginseng, but its effect on AR is unknown.</div></div><div><h3>Objective</h3><div>This study investigated the therapeutic potential of Rg5 in toluene diisocyanate (TDI)-induced AR and explored its potential mechanism involving JAK2/SATAT3/BCL-2 and MAPK signaling pathways as well as nasal microbiota regulation.</div></div><div><h3>Methods</h3><div>AR model was established by TDI sensitization and different doses of Rg5 were administered to assess symptom scores, IgE, His and cytokine levels. Nasal mucosal tissues and lung tissues were analyzed histopathologically for key proteins in the JAK2/STAT3/BCL-2 and MAPK pathways in the nasal mucosa. Nasal microbiota composition was assessed using 16S rRNA sequencing and signaling pathway correlation analysis was performed.</div></div><div><h3>Results</h3><div>Rg5 significantly reduces IgE, His, and pro-inflammatory factors, increases anti-inflammatory factors, mitigates damage to the nasal mucosa and lung tissues, thereby alleviates nasal symptoms. It suppresses the activation of JAK2/STAT3 and MAPK pathways and upregulates BCL-2 expression. It also increases the abundance of <em>Actinobacteria</em> and <em>Acidobacteria</em>, decreases that of <em>Bacteroidetes</em> and <em>Desulfobacteria</em>, and restores the diversity of nasal microbiota. Rg5 ameliorates AR symptoms by enriching beneficial bacteria (e.g., <em>Campylobacterota</em>, <em>Patescibacteria</em>, and <em>Acidobacteriota</em>), regulating cytokine levels, and synergistically modulating the JAK2/STAT3/BCL-2 and MAPK pathways.</div></div><div><h3>Conclusion</h3><div>Ginsenoside Rg5 acts synergistically through the JAK2/STAT3/BCL-2 and MAPK signaling pathways while restoring nasal microbiota homeostasis and attenuating TDI-induced AR symptoms, highlighting its potential as a novel therapeutic agent for AR.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 3","pages":"Article 100984"},"PeriodicalIF":5.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147807304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}