Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.11.009
Do Su Lim , Sung Ho Ahn , Wonjun Cho , Hyeon Ji Gwon , Jun Hwi Ko , Min Kyung Pyo , A.M. Abd El-Aty , Soon Auck Hong , Jong Wook Shin , Ji Hoon Jeong , Tae Woo Jung
Aim
The current study aimed to investigate the effects of the ginsenoside Rg5 (Rg5) on aging-induced apoptosis and ferroptosis in tenocytes and explore its mechanism of action.
Methods
The expression of various proteins related to this study was assessed via Western blotting. Cell viability and caspase 3 activity assays were conducted. Cellular iron content and oxidative stress markers in tenocytes were evaluated via commercial assay kits. siRNA transfection and inhibitors were used to explore the mechanism involved. In in vivo studies, H&E staining was performed to analyze the histopathology of the tendon tissue of mice.
Results
Rg5 treatment attenuated apoptosis, ferroptosis, ER stress, and oxidative stress in D-galactose-treated tenocytes. Moreover, it mitigated ECM degradation and enhanced cell migration in tenocytes in the presence of D-galactose. Rg5 treatment dose-dependently increased SIRT6 expression and the levels of autophagy markers, such as those associated with LC3 conversion and p62 degradation. siRNA-mediated suppression of SIRT6 or 3-MA, an autophagy inhibitor, reduced the effects of Rg5 on D-galactose-treated tenocytes. Rg5 administration improved tissue damage as well as ER stress and ferroptosis markers in the Achilles tendons of mouse models established by local injection of D-galactose and collagenase type I. In addition to the in vitro results, it promoted SIRT6 expression and p62 degradation in in vivo studies.
Conclusion
These results suggest that Rg5 attenuates ER stress and oxidative stress through the SIRT6/autophagy axis, thereby mitigating ferroptosis and apoptosis in aging-conditioned tenocytes. The present study sheds light on a novel therapeutic strategy for aging-mediated tendinopathy involving the use of Rg5.
{"title":"Ginsenoside Rg5 mitigates tenocyte death via SIRT6/autophagy-dependent signaling in an aging model","authors":"Do Su Lim , Sung Ho Ahn , Wonjun Cho , Hyeon Ji Gwon , Jun Hwi Ko , Min Kyung Pyo , A.M. Abd El-Aty , Soon Auck Hong , Jong Wook Shin , Ji Hoon Jeong , Tae Woo Jung","doi":"10.1016/j.jgr.2025.11.009","DOIUrl":"10.1016/j.jgr.2025.11.009","url":null,"abstract":"<div><h3>Aim</h3><div>The current study aimed to investigate the effects of the ginsenoside Rg5 (Rg5) on aging-induced apoptosis and ferroptosis in tenocytes and explore its mechanism of action.</div></div><div><h3>Methods</h3><div>The expression of various proteins related to this study was assessed <em>via</em> Western blotting. Cell viability and caspase 3 activity assays were conducted. Cellular iron content and oxidative stress markers in tenocytes were evaluated <em>via</em> commercial assay kits. siRNA transfection and inhibitors were used to explore the mechanism involved. In <em>in vivo</em> studies, H&E staining was performed to analyze the histopathology of the tendon tissue of mice.</div></div><div><h3>Results</h3><div>Rg5 treatment attenuated apoptosis, ferroptosis, ER stress, and oxidative stress in D-galactose-treated tenocytes. Moreover, it mitigated ECM degradation and enhanced cell migration in tenocytes in the presence of D-galactose. Rg5 treatment dose-dependently increased SIRT6 expression and the levels of autophagy markers, such as those associated with LC3 conversion and p62 degradation. siRNA-mediated suppression of SIRT6 or 3-MA, an autophagy inhibitor, reduced the effects of Rg5 on D-galactose-treated tenocytes. Rg5 administration improved tissue damage as well as ER stress and ferroptosis markers in the Achilles tendons of mouse models established by local injection of D-galactose and collagenase type I. In addition to the <em>in vitro</em> results, it promoted SIRT6 expression and p62 degradation in <em>in vivo</em> studies.</div></div><div><h3>Conclusion</h3><div>These results suggest that Rg5 attenuates ER stress and oxidative stress through the SIRT6/autophagy axis, thereby mitigating ferroptosis and apoptosis in aging-conditioned tenocytes. The present study sheds light on a novel therapeutic strategy for aging-mediated tendinopathy involving the use of Rg5.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100921"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877038","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.002
Rahmi Lee , McKennon J. Wiles , Ellison R. Black , Seung Hyun Roh , Evelina Bouckova , Madison H. Wustrau , Joshua C. Flowers , Paige E. Vetter , Jaehoon Lee , Byung-Cheol Han , Seonil Kim
Background
Stress affects brain functions, which leads to the development of mental disorders. There is increasing focus on the role of nutritional, herbal and nutraceutical compounds on mental and cognitive functioning. Interestingly, studies suggest that American ginseng (Panax quinquefolius L.) extracts (G1899) improve cognition.
Methods
We examined whether G1899 showed protective effects on stress-induced behavioral changes in animals. 200 mg/kg G1899 was orally administered daily for 4 weeks to 2-3-month-old female and male mice before inducing stress. To induce acute stress in animals, we intraperitoneally injected a low dose of lipopolysaccharides (LPS) (10 μg/kg), and saline was used as a control. We also used chronic restraint stress (CRS) as a chronic stress model in mice. After LPS injection or CRS, multiple behavioral assays were carried out – a sucrose preference test, an open filed test, reciprocal social interaction, contextual fear conditioning, and a tail suspension test – to determine whether acute or chronic stress affected animals' behaviors and whether G1899 had protective effects against stress-induced behavioral dysfunction.
Results
We found that both LPS injection and CRS induced stress-related behavioral dysfunction, including depression-like behavior, anhedonia, social dysfunction, and fear memory impairments in mice. However, G1899 was sufficient to reverse stress-induced behavioral abnormalities in animals. Our data further suggested that G1899 reduced the activity of hippocampal neurons by suppressing glutamatergic activity.
Conclusion
G1899 supplements can be protective against both acute and chronic stress in mice by suppressing neuronal and synaptic activity.
{"title":"American ginseng (Panax quinquefolius L.) extracts (G1899) reverse stress-induced behavioral abnormalities in mice","authors":"Rahmi Lee , McKennon J. Wiles , Ellison R. Black , Seung Hyun Roh , Evelina Bouckova , Madison H. Wustrau , Joshua C. Flowers , Paige E. Vetter , Jaehoon Lee , Byung-Cheol Han , Seonil Kim","doi":"10.1016/j.jgr.2025.10.002","DOIUrl":"10.1016/j.jgr.2025.10.002","url":null,"abstract":"<div><h3>Background</h3><div>Stress affects brain functions, which leads to the development of mental disorders. There is increasing focus on the role of nutritional, herbal and nutraceutical compounds on mental and cognitive functioning. Interestingly, studies suggest that American ginseng (<em>Panax quinquefolius</em> L.) extracts (G1899) improve cognition.</div></div><div><h3>Methods</h3><div>We examined whether G1899 showed protective effects on stress-induced behavioral changes in animals. 200 mg/kg G1899 was orally administered daily for 4 weeks to 2-3-month-old female and male mice before inducing stress. To induce acute stress in animals, we intraperitoneally injected a low dose of lipopolysaccharides (LPS) (10 μg/kg), and saline was used as a control. We also used chronic restraint stress (CRS) as a chronic stress model in mice. After LPS injection or CRS, multiple behavioral assays were carried out – a sucrose preference test, an open filed test, reciprocal social interaction, contextual fear conditioning, and a tail suspension test – to determine whether acute or chronic stress affected animals' behaviors and whether G1899 had protective effects against stress-induced behavioral dysfunction.</div></div><div><h3>Results</h3><div>We found that both LPS injection and CRS induced stress-related behavioral dysfunction, including depression-like behavior, anhedonia, social dysfunction, and fear memory impairments in mice. However, G1899 was sufficient to reverse stress-induced behavioral abnormalities in animals. Our data further suggested that G1899 reduced the activity of hippocampal neurons by suppressing glutamatergic activity.</div></div><div><h3>Conclusion</h3><div>G1899 supplements can be protective against both acute and chronic stress in mice by suppressing neuronal and synaptic activity.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100905"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877049","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.005
Chuan Li , Yuhao Zhou , Yuxi Nie , Jingran Fu , Jia Zeng , Shike Zhang , Liang Han , Zhuojia Li , Hongcan Yang , Shujue Li , Beixin Yu , Xiaoling Ying , Wenqi Wu
Background
Kidney stone disease (KSD), notably characterized by heightened oxidative stress and cell death within renal tubular epithelial cells due to high oxalate. Ginsenoside Ro (Ro), a scarce oleanane-type saponin isolated from Panax ginseng Mey. and Achyranthes bidentata Bl., has garnered attention for the anti-tumor, anti-oxidant, and anti-inflammatory properties. This study aims to investigate the protective effects and mechanisms of Ro on crystal-induced renal injury in vivo and in vitro.
Materials and methods
In vitro, we assessed renal injury, renal crystal deposition, and inflammatory infiltration in a glyoxylic acid (Gly)-induced stone formation mouse model, with administration of Ro. The protective effects of Ro on proximal tubular epithelial cell line HK-2 damaged by hyperoxaluria were assessed via MTS assay and live/dead cell staining in vivo. Additionally, we examined reactive oxygen species (ROS) levels and crystal adhesion-related proteins. Subsequently, we identified ZnT1 as the target of Ro through RNA-seq, immunohistochemical (IHC) staining, Western blotting (WB), molecular docking, molecular dynamics simulations, bio‐layer interferometry (BLI) and cellular thermal shift assay (CETSA). Further, we constructed HK-2 cells over-expressing and knocking out of ZnT1 to evaluated cellular damage and crystal adhesion effects. Finally, the role of Ro in high oxalate-induced cuproptosis in HK-2 was examined via cuproptosis-related events, including DLAT oligomerization, cuproptosis-associated proteins FDX1 and HSP70, mitochondrial ROS levels, JC-1 staining, and GSH levels.
Results
Ro effectively mitigated renal injury induced by Gly in mice. Moreover, it notably ameliorated renal crystal deposition and infiltration of F4/80-positive macrophages observed in Gly mice. Additionally, in vitro studies demonstrated that Ro alleviated oxidative damage and crystal adhesion induced by high oxalate in HK-2 cells. Mechanistically, Ro significantly suppressed ZnT1 expression, and notably, over-expression of ZnT1 reversed the inhibitory of Ro on NaOx-induced proliferation suppression, crystal adhesion, and augmented ROS generation in HK-2 cells. Additionally, NaOx elevated cuproptosis in HK-2 cells, and this elevation was blocked by ZnT1 over-expression, which in turn was reversed by TTM, a cuproptosis inhibitor.
Conclusion
This study provided evidence that Ro mitigated cuproptosis HK-2 cells induced by high oxalate through inhibiting ZnT1, thus effectively suppressing oxidative stress and crystal deposition triggered by high oxalate.
{"title":"Ginsenoside Ro alleviated cuproptosis induced by high oxalate via inhibiting zinc transporter ZnT1 in renal tubular epithelial cells","authors":"Chuan Li , Yuhao Zhou , Yuxi Nie , Jingran Fu , Jia Zeng , Shike Zhang , Liang Han , Zhuojia Li , Hongcan Yang , Shujue Li , Beixin Yu , Xiaoling Ying , Wenqi Wu","doi":"10.1016/j.jgr.2025.10.005","DOIUrl":"10.1016/j.jgr.2025.10.005","url":null,"abstract":"<div><h3>Background</h3><div>Kidney stone disease (KSD), notably characterized by heightened oxidative stress and cell death within renal tubular epithelial cells due to high oxalate. Ginsenoside Ro (Ro), a scarce oleanane-type saponin isolated from <em>Panax ginseng</em> Mey. and <em>Achyranthes bidentata</em> Bl., has garnered attention for the anti-tumor, anti-oxidant, and anti-inflammatory properties. This study aims to investigate the protective effects and mechanisms of Ro on crystal-induced renal injury <em>in vivo</em> and <em>in vitro</em>.</div></div><div><h3>Materials and methods</h3><div><em>In vitro</em>, we assessed renal injury, renal crystal deposition, and inflammatory infiltration in a glyoxylic acid (Gly)-induced stone formation mouse model, with administration of Ro. The protective effects of Ro on proximal tubular epithelial cell line HK-2 damaged by hyperoxaluria were assessed via MTS assay and live/dead cell staining <em>in vivo</em>. Additionally, we examined reactive oxygen species (ROS) levels and crystal adhesion-related proteins. Subsequently, we identified ZnT1 as the target of Ro through RNA-seq, immunohistochemical (IHC) staining, Western blotting (WB), molecular docking, molecular dynamics simulations, bio‐layer interferometry (BLI) and cellular thermal shift assay (CETSA). Further, we constructed HK-2 cells over-expressing and knocking out of ZnT1 to evaluated cellular damage and crystal adhesion effects. Finally, the role of Ro in high oxalate-induced cuproptosis in HK-2 was examined via cuproptosis-related events, including DLAT oligomerization, cuproptosis-associated proteins FDX1 and HSP70, mitochondrial ROS levels, JC-1 staining, and GSH levels.</div></div><div><h3>Results</h3><div>Ro effectively mitigated renal injury induced by Gly in mice. Moreover, it notably ameliorated renal crystal deposition and infiltration of F4/80-positive macrophages observed in Gly mice. Additionally, <em>in vitro</em> studies demonstrated that Ro alleviated oxidative damage and crystal adhesion induced by high oxalate in HK-2 cells. Mechanistically, Ro significantly suppressed ZnT1 expression, and notably, over-expression of ZnT1 reversed the inhibitory of Ro on NaOx-induced proliferation suppression, crystal adhesion, and augmented ROS generation in HK-2 cells. Additionally, NaOx elevated cuproptosis in HK-2 cells, and this elevation was blocked by ZnT1 over-expression, which in turn was reversed by TTM, a cuproptosis inhibitor.</div></div><div><h3>Conclusion</h3><div>This study provided evidence that Ro mitigated cuproptosis HK-2 cells induced by high oxalate through inhibiting ZnT1, thus effectively suppressing oxidative stress and crystal deposition triggered by high oxalate.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100908"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877057","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.003
Linlin Gao , Fushuang Zheng , Zhiling Fu , Wei Wang
Background
Sepsis-induced acute lung injury (ALI) is a life-threatening condition with high mortality and limited effective treatments. Aging of alveolar type II (AT2) epithelial cells and mitochondrial dysfunction are key contributors to ALI pathogenesis. Ginsenoside Rb1, a major bioactive component of ginseng, has shown potential in modulating cellular senescence and mitochondrial health. This study aimed to evaluate the therapeutic efficacy of Rb1-loaded lung tissue-derived decellularized extracellular matrix hydrogel (dECM-gel) in alleviating sepsis-induced ALI.
Methods and results
Rb1-loaded dECM-gel was formulated and characterized for its rheological properties. In vitro, primary AT2 cells were treated with lipopolysaccharide (LPS) to mimic ALI conditions. The impact of Rb1-loaded dECM-gel on cellular senescence, mitochondrial function, and oxidative stress was assessed using β-galactosidase staining, JC-1 dye for mitochondrial membrane potential, ATP quantification assays, and transmission electron microscopy. Results demonstrated that Rb1-loaded dECM-gel significantly reduced AT2 cell senescence, improved mitochondrial function via activation of the mitochondrial unfolded protein response (mtUPR), and alleviated mitochondrial structural damage. In vivo, a murine model of sepsis-induced ALI was used to evaluate therapeutic outcomes. Treatment with Rb1-loaded dECM-gel improved lung histopathology, decreased oxidative stress, and reduced apoptosis, largely through activation of the AMPK/SIRT1 signaling pathway.
Conclusion
Rb1-loaded dECM-gel mitigates sepsis-induced ALI by enhancing mtUPR and activating the AMPK/SIRT1 pathway, offering a promising therapeutic strategy for lung injury. These findings underscore the potential of ginsenoside-based biomaterials in the clinical management of ALI.
{"title":"Ginsenoside Rb1-enhanced decellularized extracellular matrix hydrogels ameliorates mitochondrial dysfunction and cellular aging in sepsis-induced acute lung injury","authors":"Linlin Gao , Fushuang Zheng , Zhiling Fu , Wei Wang","doi":"10.1016/j.jgr.2025.10.003","DOIUrl":"10.1016/j.jgr.2025.10.003","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis-induced acute lung injury (ALI) is a life-threatening condition with high mortality and limited effective treatments. Aging of alveolar type II (AT2) epithelial cells and mitochondrial dysfunction are key contributors to ALI pathogenesis. Ginsenoside Rb1, a major bioactive component of ginseng, has shown potential in modulating cellular senescence and mitochondrial health. This study aimed to evaluate the therapeutic efficacy of Rb1-loaded lung tissue-derived decellularized extracellular matrix hydrogel (dECM-gel) in alleviating sepsis-induced ALI.</div></div><div><h3>Methods and results</h3><div>Rb1-loaded dECM-gel was formulated and characterized for its rheological properties. In vitro, primary AT2 cells were treated with lipopolysaccharide (LPS) to mimic ALI conditions. The impact of Rb1-loaded dECM-gel on cellular senescence, mitochondrial function, and oxidative stress was assessed using β-galactosidase staining, JC-1 dye for mitochondrial membrane potential, ATP quantification assays, and transmission electron microscopy. Results demonstrated that Rb1-loaded dECM-gel significantly reduced AT2 cell senescence, improved mitochondrial function via activation of the mitochondrial unfolded protein response (mtUPR), and alleviated mitochondrial structural damage. In vivo, a murine model of sepsis-induced ALI was used to evaluate therapeutic outcomes. Treatment with Rb1-loaded dECM-gel improved lung histopathology, decreased oxidative stress, and reduced apoptosis, largely through activation of the AMPK/SIRT1 signaling pathway.</div></div><div><h3>Conclusion</h3><div>Rb1-loaded dECM-gel mitigates sepsis-induced ALI by enhancing mtUPR and activating the AMPK/SIRT1 pathway, offering a promising therapeutic strategy for lung injury. These findings underscore the potential of ginsenoside-based biomaterials in the clinical management of ALI.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100906"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877056","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.11.010
Su-Min Baek , Young-Jin Lee , Jae-Hyuk Yim , Tae-Un Kim , Woo Jun Kim , Seoung-Woo Lee , Hee-Yeon Kim , Kyung-Ku Kang , Kyeong-Min Lee , Seong-Kyoon Choi , Sung Dae Kim , Man-Hee Rhee , Jin-Kyu Park
Background
Impaired intestinal mucosal barrier in alcoholic liver disease leads to the entry of toxic substances into the liver parenchyma. Ingestion of microplastics (MPs; plastic particles sized <5 mm) can induce inflammation, metabolic disorders, oxidative stress, and cancer. Red ginseng extract (RGE) is a widely used herbal medicine globally. The effects of RGE on the accumulation of MPs and the underlying mechanisms remain unclear.
Methods
Nine-week-old male wild-type C57BL/6 mice were fed a control liquid diet or ethanol diet with or without MP and RGE. MPs (fluorescent-tagged 2.16-μm polystyrene MP; dose: 0.1 mg/kg body weight) and RGE (dose: 250 or 500 mg/kg body weight) were orally administered five times a week.
Results
RGE treatment markedly reduced MP accumulation in the liver and intestines. In the intestines, RGE protected tight junctions, as shown by ZO-1 and F-actin expression, and prevented MP translocation into the lamina propria. It also inhibited ethanol- and MP-induced villi fusion, epithelial detachment, and vacuolization. In the liver, RGE attenuated ethanol-mediated steatosis, lobular inflammation, and ballooning degeneration. In vitro, RGE restored tight junction integrity in Caco-2 cells by upregulating ZO-1 while reducing MP accumulation. However, its effect on goblet cell differentiation (MUC-2) in HT-29 cells was minimal, suggesting that in vivo goblet cell regeneration occurred secondarily to tight junction protection.
Conclusion
Disruption of the gut–liver axis leads to increased translocation of MPs into the lamina propria and their secondary accumulation in the intestines and liver. RGE inhibits the accumulation of MPs by protecting the intestinal epithelial mucosal barrier.
{"title":"Korean red ginseng extract inhibits microplastic translocation via the gut−liver axis by ameliorating alcohol-induced intestinal disruption","authors":"Su-Min Baek , Young-Jin Lee , Jae-Hyuk Yim , Tae-Un Kim , Woo Jun Kim , Seoung-Woo Lee , Hee-Yeon Kim , Kyung-Ku Kang , Kyeong-Min Lee , Seong-Kyoon Choi , Sung Dae Kim , Man-Hee Rhee , Jin-Kyu Park","doi":"10.1016/j.jgr.2025.11.010","DOIUrl":"10.1016/j.jgr.2025.11.010","url":null,"abstract":"<div><h3>Background</h3><div>Impaired intestinal mucosal barrier in alcoholic liver disease leads to the entry of toxic substances into the liver parenchyma. Ingestion of microplastics (MPs; plastic particles sized <5 mm) can induce inflammation, metabolic disorders, oxidative stress, and cancer. Red ginseng extract (RGE) is a widely used herbal medicine globally. The effects of RGE on the accumulation of MPs and the underlying mechanisms remain unclear.</div></div><div><h3>Methods</h3><div>Nine-week-old male wild-type C57BL/6 mice were fed a control liquid diet or ethanol diet with or without MP and RGE. MPs (fluorescent-tagged 2.16-μm polystyrene MP; dose: 0.1 mg/kg body weight) and RGE (dose: 250 or 500 mg/kg body weight) were orally administered five times a week.</div></div><div><h3>Results</h3><div>RGE treatment markedly reduced MP accumulation in the liver and intestines. In the intestines, RGE protected tight junctions, as shown by ZO-1 and F-actin expression, and prevented MP translocation into the lamina propria. It also inhibited ethanol- and MP-induced villi fusion, epithelial detachment, and vacuolization. In the liver, RGE attenuated ethanol-mediated steatosis, lobular inflammation, and ballooning degeneration. <em>In vitro</em>, RGE restored tight junction integrity in Caco-2 cells by upregulating ZO-1 while reducing MP accumulation. However, its effect on goblet cell differentiation (MUC-2) in HT-29 cells was minimal, suggesting that <em>in vivo</em> goblet cell regeneration occurred secondarily to tight junction protection.</div></div><div><h3>Conclusion</h3><div>Disruption of the gut–liver axis leads to increased translocation of MPs into the lamina propria and their secondary accumulation in the intestines and liver. RGE inhibits the accumulation of MPs by protecting the intestinal epithelial mucosal barrier.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100922"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877039","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.009
Cheol Park , Hee-Jae Cha , Kyoung-Seob Song , Heui-Soo Kim , EunJin Bang , Hyesook Lee , Cheng-Yun Jin , Gi-Young Kim , Yung Hyun Choi
{"title":"Corrigendum to “Nrf2-mediated activation of HO-1 is required in the blocking effect of compound K, a ginseng saponin metabolite, against oxidative stress damage in ARPE-19 human retinal pigment epithelial cells” [J. Ginseng Res. 47 (2) (March 2023) 311]","authors":"Cheol Park , Hee-Jae Cha , Kyoung-Seob Song , Heui-Soo Kim , EunJin Bang , Hyesook Lee , Cheng-Yun Jin , Gi-Young Kim , Yung Hyun Choi","doi":"10.1016/j.jgr.2025.10.009","DOIUrl":"10.1016/j.jgr.2025.10.009","url":null,"abstract":"","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100912"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877040","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.09.001
Xuan Zhao , Xinrui Li , Xuhui Jia , Yan Gao
Background
Ginsenosides, the main active compounds in American ginseng, have notable pharmacological effects, with rare ginsenosides offering higher bioavailability and bioactivity despite low abundance. Cordyceps militaris, an edible fungus, produces cordycepin and secretes enzymes like β-glucosidase that convert and enhance ginsenoside content. This study employed solid-state fermentation of American ginseng with C. militaris to investigate ginsenoside conversion and enrichment, alongside analyzing changes in cordycepin, gene expression, and metabolites during fermentation.
Materials and methods
In this study, 30 % powdered ginseng was added to the C. militaris culture medium, with samples collected on different days for HPLC analysis of ginsenosides and cordycepin. Transcriptome sequencing and metabolomics analysis of C. militaris was performed on day 40 to investigate the pathways and mechanisms involved in the transformation and enrichment of these components.
Results
HPLC analysis revealed that cordycepin levels in C. militaris cultured with American ginseng increased over time. Rare ginsenoside CK rose from undetectable to 11.81 mg, alongside significant increases in other rare ginsenosides. Mass spectrometry suggests ginsenoside CK is biosynthesized from Rb1 through intermediates Rd and F2. Transcriptome sequencing and metabolomics analysis revealed elevated expression of β-glucosidase and cordycepin synthesis genes. β-glucosidase is involved in carbohydrate and amino acid metabolism pathways, promoting substrate accumulation and providing energy for cordycepin synthesis.
Conclusion
This study demonstrates that co-culture of American ginseng with C. militaris enables bidirectional biotransformation: fungal enzymes convert ginsenosides into rare ginsenosides, while ginseng nutrients upregulate cordycepin biosynthesis. It offers a novel, eco-friendly approach for targeted transformation and enrichment of active ingredients.
{"title":"Multi-omics and compositional analysis of bidirectional solid fermentation products from Cordyceps militaris and Panax quinquefolius L","authors":"Xuan Zhao , Xinrui Li , Xuhui Jia , Yan Gao","doi":"10.1016/j.jgr.2025.09.001","DOIUrl":"10.1016/j.jgr.2025.09.001","url":null,"abstract":"<div><h3>Background</h3><div>Ginsenosides, the main active compounds in American ginseng, have notable pharmacological effects, with rare ginsenosides offering higher bioavailability and bioactivity despite low abundance. <em>Cordyceps militaris</em>, an edible fungus, produces cordycepin and secretes enzymes like β-glucosidase that convert and enhance ginsenoside content. This study employed solid-state fermentation of American ginseng with <em>C. militaris</em> to investigate ginsenoside conversion and enrichment, alongside analyzing changes in cordycepin, gene expression, and metabolites during fermentation.</div></div><div><h3>Materials and methods</h3><div>In this study, 30 % powdered ginseng was added to the <em>C. militaris</em> culture medium, with samples collected on different days for HPLC analysis of ginsenosides and cordycepin. Transcriptome sequencing and metabolomics analysis of <em>C. militaris</em> was performed on day 40 to investigate the pathways and mechanisms involved in the transformation and enrichment of these components.</div></div><div><h3>Results</h3><div>HPLC analysis revealed that cordycepin levels in <em>C. militaris</em> cultured with American ginseng increased over time. Rare ginsenoside CK rose from undetectable to 11.81 mg, alongside significant increases in other rare ginsenosides. Mass spectrometry suggests ginsenoside CK is biosynthesized from Rb1 through intermediates Rd and F2. Transcriptome sequencing and metabolomics analysis revealed elevated expression of β-glucosidase and cordycepin synthesis genes. β-glucosidase is involved in carbohydrate and amino acid metabolism pathways, promoting substrate accumulation and providing energy for cordycepin synthesis.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that co-culture of American ginseng with <em>C. militaris</em> enables bidirectional biotransformation: fungal enzymes convert ginsenosides into rare ginsenosides, while ginseng nutrients upregulate cordycepin biosynthesis. It offers a novel, eco-friendly approach for targeted transformation and enrichment of active ingredients.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100900"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877050","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.006
Yuan Yee Lee , Abdul Wahab Akram , Evelyn Saba , Hyung-Kyu Chae , Min-Goo Seo , Sung Dae Kim , Sang-Joon Park , Dongmi Kwak , Man Hee Rhee
Background
Sepsis is a life-threatening condition characterized by systemic inflammation and thrombo-inflammation, which trigger platelet activation and platelet–leukocyte aggregate (PLA) formation. While Rg3-enriched red ginseng extract (Rg3-RGE) has demonstrated anti-inflammatory and antithrombotic properties, its role in modulating PLAs during sepsis remains poorly understood.
Methods
The in vivo effects of Rg3-RGE were analyzed in a lipopolysaccharide (LPS)-induced murine model of sepsis. Flow cytometry was used to evaluate platelet–leukocyte activation markers. Confocal and scanning electron microscopy (SEM) provided visual evidence of aggregate formation. ELISA was used to quantify plasma levels of tissue factor (TF) and platelet factor 4 (PF4). HPLC analysis revealed the presence of Rb1, Rg3 [20(S) and 20(R)], Rc, Rd, Rf, Rh1, Rb2, and Rg2 [20(S)] in Rg3-RGE. Network pharmacology was employed to identify target interactions and assess their involvement in the thrombo-inflammatory pathway.
Results
Rg3-RGE significantly reduced the activated platelets (CD41+CD62P+), platelet–neutrophil aggregates (PNAs; CD41+Ly6G+), and platelet–monocyte aggregates (PMAs; CD41+CD115+). Confocal imaging confirmed a reduction in PNAs. SEM revealed decreased fibrin-like structures and fewer platelet–leukocyte interactions. Rg3-RGE lowered plasma TF levels, indicating a potential effect on the coagulation cascade, though PF4 levels were not significantly altered. Network pharmacology analysis of ginsenosides in Rg3-RGE identified 235 overlapping targets associated with sepsis, inflammation, platelet activation, and PLA formation. Enrichment analysis revealed key thrombo-inflammatory pathways, including platelet activation, MAPK signaling, PI3K-Akt signaling, sphingosine-1-phosphate receptor signaling, and EGFR signaling.
{"title":"Ginsenoside Rg3-enriched red ginseng extract mitigates sepsis by inhibiting platelet–leukocyte aggregates and regulates thrombo-inflammatory pathways","authors":"Yuan Yee Lee , Abdul Wahab Akram , Evelyn Saba , Hyung-Kyu Chae , Min-Goo Seo , Sung Dae Kim , Sang-Joon Park , Dongmi Kwak , Man Hee Rhee","doi":"10.1016/j.jgr.2025.10.006","DOIUrl":"10.1016/j.jgr.2025.10.006","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis is a life-threatening condition characterized by systemic inflammation and thrombo-inflammation, which trigger platelet activation and platelet–leukocyte aggregate (PLA) formation. While Rg3-enriched red ginseng extract (Rg3-RGE) has demonstrated anti-inflammatory and antithrombotic properties, its role in modulating PLAs during sepsis remains poorly understood.</div></div><div><h3>Methods</h3><div>The <em>in vivo</em> effects of Rg3-RGE were analyzed in a lipopolysaccharide (LPS)-induced murine model of sepsis. Flow cytometry was used to evaluate platelet–leukocyte activation markers. Confocal and scanning electron microscopy (SEM) provided visual evidence of aggregate formation. ELISA was used to quantify plasma levels of tissue factor (TF) and platelet factor 4 (PF4). HPLC analysis revealed the presence of Rb1, Rg3 [20(S) and 20(R)], Rc, Rd, Rf, Rh1, Rb2, and Rg2 [20(S)] in Rg3-RGE. Network pharmacology was employed to identify target interactions and assess their involvement in the thrombo-inflammatory pathway.</div></div><div><h3>Results</h3><div>Rg3-RGE significantly reduced the activated platelets (CD41+CD62P+), platelet–neutrophil aggregates (PNAs; CD41+Ly6G+), and platelet–monocyte aggregates (PMAs; CD41+CD115+). Confocal imaging confirmed a reduction in PNAs. SEM revealed decreased fibrin-like structures and fewer platelet–leukocyte interactions. Rg3-RGE lowered plasma TF levels, indicating a potential effect on the coagulation cascade, though PF4 levels were not significantly altered. Network pharmacology analysis of ginsenosides in Rg3-RGE identified 235 overlapping targets associated with sepsis, inflammation, platelet activation, and PLA formation. Enrichment analysis revealed key thrombo-inflammatory pathways, including platelet activation, MAPK signaling, PI3K-Akt signaling, sphingosine-1-phosphate receptor signaling, and EGFR signaling.</div></div><div><h3>Conclusion</h3><div>Rg3-RGE effectively inhibits platelet–leukocyte aggregate formation and mitigates sepsis-induced platelet–leukocyte interactions.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100909"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877071","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.11.007
Hyun Seung Lee , Heung-Woo Park
Background
Airway epithelial cells initiate asthma-related inflammation, making them key therapeutic targets. While some ginsenosides, the principal active constituents of Panax ginseng, are known to modulate epithelial inflammation, the role of ginsenoside Rg1 in this context remains underexplored. This study investigated the therapeutic effects of ginsenoside Rg1 on airway inflammation and airway hyperresponsiveness (AHR) in a murine asthma model induced by co-exposure to Dermatophagoides pteronyssinus (Dp) and diesel exhaust particles (DEP).
Methods
BALB/c mice were exposed intranasally to Dp and DEP with or without ginsenoside Rg1 treatment. AHR, inflammatory cell counts in bronchoalveolar lavage fluid, serum IgG1 levels, lung histopathology, and cytokine levels were assessed. Lung Th2/Th17 cells and ILC2/ILC3 populations were analyzed by flow cytometry. Mechanistic studies were conducted using MLE-12 lung epithelial cells and ILC2 co-cultures.
Results
Co-exposure to Dp and DEP significantly increased AHR, eosinophilic inflammation, Th2/Th17 responses, and ILC2/ILC3 populations. Ginsenoside Rg1 treatment markedly attenuated AHR, reduced eosinophils and serum Dp-specific IgG1, and decreased frequencies of IL-13+ ILC2s and IL-17+ ILC3s. IL-33 and IL-1β levels in lung tissue were also significantly reduced by Rg1. In MLE-12 cells, Rg1 suppressed IL-33 and phosphorylated STAT6 expression, mirroring the effects of a STAT6 inhibitor. Furthermore, Rg1 reduced IL-13 and IL-5 secretion from ILC2s co-cultured with MLE-12 cells.
Conclusion
Ginsenoside Rg1 mitigates Dp/DEP-induced airway inflammation by downregulating Th2/Th17 and ILC2/ILC3 responses, potentially via the IL-33–STAT6 axis in airway epithelial cells.
{"title":"Ginsenoside Rg1 attenuates asthma features in mice co-exposed to house dust mite allergen and diesel exhaust particle by modulating epithelial ILC2 interactions","authors":"Hyun Seung Lee , Heung-Woo Park","doi":"10.1016/j.jgr.2025.11.007","DOIUrl":"10.1016/j.jgr.2025.11.007","url":null,"abstract":"<div><h3>Background</h3><div>Airway epithelial cells initiate asthma-related inflammation, making them key therapeutic targets. While some ginsenosides, the principal active constituents of <em>Panax ginseng</em>, are known to modulate epithelial inflammation, the role of ginsenoside Rg1 in this context remains underexplored. This study investigated the therapeutic effects of ginsenoside Rg1 on airway inflammation and airway hyperresponsiveness (AHR) in a murine asthma model induced by co-exposure to <em>Dermatophagoides pteronyssinus</em> (Dp) and diesel exhaust particles (DEP).</div></div><div><h3>Methods</h3><div>BALB/c mice were exposed intranasally to Dp and DEP with or without ginsenoside Rg1 treatment. AHR, inflammatory cell counts in bronchoalveolar lavage fluid, serum IgG1 levels, lung histopathology, and cytokine levels were assessed. Lung Th2/Th17 cells and ILC2/ILC3 populations were analyzed by flow cytometry. Mechanistic studies were conducted using MLE-12 lung epithelial cells and ILC2 co-cultures.</div></div><div><h3>Results</h3><div>Co-exposure to Dp and DEP significantly increased AHR, eosinophilic inflammation, Th2/Th17 responses, and ILC2/ILC3 populations. Ginsenoside Rg1 treatment markedly attenuated AHR, reduced eosinophils and serum Dp-specific IgG1, and decreased frequencies of IL-13+ ILC2s and IL-17+ ILC3s. IL-33 and IL-1β levels in lung tissue were also significantly reduced by Rg1. In MLE-12 cells, Rg1 suppressed IL-33 and phosphorylated STAT6 expression, mirroring the effects of a STAT6 inhibitor. Furthermore, Rg1 reduced IL-13 and IL-5 secretion from ILC2s co-cultured with MLE-12 cells.</div></div><div><h3>Conclusion</h3><div>Ginsenoside Rg1 mitigates Dp/DEP-induced airway inflammation by downregulating Th2/Th17 and ILC2/ILC3 responses, potentially via the IL-33–STAT6 axis in airway epithelial cells.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100919"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877036","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}
Pub Date : 2026-01-01DOI: 10.1016/j.jgr.2025.10.007
Ye Ji Kim , Md Shiblee Sadik Sabuj , Myung-Kon Kim , Joonseok Lee , Ryunhee Kim , Seung Hyun Lee , Jin Min Oh , Hyeon Gyeong Ro , In-Shik Kim , Dongchoon Ahn , Md Rashedunnabi Akanda , Hyun-Jin Tae , Byung-Yong Park
Background
Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is a severe condition linked to higher morbidity and mortality. Panax ginseng (PG) possesses renoprotective properties; however, its inadequate bioavailability restricts its efficacy. Wild-simulated PG (WSG), processed to boost its bioactive components, exhibits improved renoprotective effects. This research examines PG, bioconverted PG (BPG), and bioconverted WSG (BWG) for their protective roles against I/R induced AKI in mice.
Methods
C57BL/6 mice underwent bilateral renal pedicle clamping via a dorsal approach for 30 min to induce ischemia, followed by clamp release and 24 h of reperfusion. Blood and kidney samples were collected at the end of the reperfusion period. Sham-operated mice underwent identical procedures without vascular clamping. Additionally, hydrogen peroxide (H2O2) induced oxidative stress in HK-2 cells.
Results
The effects of each extract were evaluated. Expression of antioxidant, inflammatory, and apoptotic factors was confirmed using western blotting, immunohistochemistry, and TUNEL assays. Both extracts improved the survival of H2O2-treated HK-2 cells and enhanced kidney function, as indicated by reduced BUN and Cr levels. Histopathological analysis showed decreased injury, preserved tubular structure, and reduced inflammation in extract-treated groups. These protective effects were linked to activation of the Nrf2/HO-1 pathway, leading to increased expression of antioxidant enzymes (CAT, GPX-1, SOD-1) and reduced malondialdehyde (MDA) levels. Moreover, the extracts downregulated pro-inflammatory cytokines (TNF-α, IL-1β), suppressed NF-κB phosphorylation, decreased Bax/Bcl-2 ratio and Caspase-3 activation, enhancing cell survival.
Conclusion
BPG and BWG remarkably ameliorated I/R-induced AKI through modulation of Nrf2/HO-1/NF-κB/Caspase-3 signaling pathway, with BWG exhibiting more substantial renoprotective effects.
{"title":"Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling","authors":"Ye Ji Kim , Md Shiblee Sadik Sabuj , Myung-Kon Kim , Joonseok Lee , Ryunhee Kim , Seung Hyun Lee , Jin Min Oh , Hyeon Gyeong Ro , In-Shik Kim , Dongchoon Ahn , Md Rashedunnabi Akanda , Hyun-Jin Tae , Byung-Yong Park","doi":"10.1016/j.jgr.2025.10.007","DOIUrl":"10.1016/j.jgr.2025.10.007","url":null,"abstract":"<div><h3>Background</h3><div>Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is a severe condition linked to higher morbidity and mortality. <em>Panax ginseng</em> (PG) possesses renoprotective properties; however, its inadequate bioavailability restricts its efficacy. Wild-simulated PG (WSG), processed to boost its bioactive components, exhibits improved renoprotective effects. This research examines PG, bioconverted PG (BPG), and bioconverted WSG (BWG) for their protective roles against I/R induced AKI in mice.</div></div><div><h3>Methods</h3><div>C57BL/6 mice underwent bilateral renal pedicle clamping via a dorsal approach for 30 min to induce ischemia, followed by clamp release and 24 h of reperfusion. Blood and kidney samples were collected at the end of the reperfusion period. Sham-operated mice underwent identical procedures without vascular clamping. Additionally, hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) induced oxidative stress in HK-2 cells.</div></div><div><h3>Results</h3><div>The effects of each extract were evaluated. Expression of antioxidant, inflammatory, and apoptotic factors was confirmed using western blotting, immunohistochemistry, and TUNEL assays. Both extracts improved the survival of H<sub>2</sub>O<sub>2</sub>-treated HK-2 cells and enhanced kidney function, as indicated by reduced BUN and Cr levels. Histopathological analysis showed decreased injury, preserved tubular structure, and reduced inflammation in extract-treated groups. These protective effects were linked to activation of the Nrf2/HO-1 pathway, leading to increased expression of antioxidant enzymes (CAT, GPX-1, SOD-1) and reduced malondialdehyde (MDA) levels. Moreover, the extracts downregulated pro-inflammatory cytokines (TNF-α, IL-1β), suppressed NF-κB phosphorylation, decreased Bax/Bcl-2 ratio and Caspase-3 activation, enhancing cell survival.</div></div><div><h3>Conclusion</h3><div>BPG and BWG remarkably ameliorated I/R-induced AKI through modulation of Nrf2/HO-1/NF-κB/Caspase-3 signaling pathway, with BWG exhibiting more substantial renoprotective effects.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100910"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877072","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}
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