Pub Date : 2025-07-01Epub Date: 2025-04-21DOI: 10.1016/j.jgr.2025.04.005
YiSi Yang , DeYu Tian , Kyoung-Jin Jang , Myeong Soo Lee , Hye Won Lee , Seung-Jin Lee , Wook-Joon Yu , Changbao Chen , Ling Li , Jong Dae Park , YoungJoo Lee
The roots of Panax ginseng, known as Korean ginseng, have been widely used worldwide for treating many diseases and general health maintenance. Korean ginseng is perceived as safe owing to its natural origin, extensive historical uses, and accumulated scientific clinical studies in humans. According to oriental medicine theory, Panax ginseng is categorized as having warm properties, while Panax quinquefolium, called American ginseng, is classified as having cool properties. Based on this, it is said that Panax ginseng might cause an elevation of body temperature, such as sensations of warmth or heat, whereas Panax quinquefolium provides cooling effects. However, scientific evidence for comparing these parallel thermogenic effects of two species is scarce. This focused review summarizes clinical trials and animal studies regarding the heat responses of two Panax species. This review aims to provide an overview of current scientific data on the thermogenic effects inducing a heat sensation and a hot feeling of Korean ginseng and American ginseng.
{"title":"The clearing-up of misunderstanding on body temperature changes and heat responses after Panax ginseng or Panax quinquefolium intake","authors":"YiSi Yang , DeYu Tian , Kyoung-Jin Jang , Myeong Soo Lee , Hye Won Lee , Seung-Jin Lee , Wook-Joon Yu , Changbao Chen , Ling Li , Jong Dae Park , YoungJoo Lee","doi":"10.1016/j.jgr.2025.04.005","DOIUrl":"10.1016/j.jgr.2025.04.005","url":null,"abstract":"<div><div>The roots of <em>Panax ginseng</em>, known as Korean ginseng, have been widely used worldwide for treating many diseases and general health maintenance. Korean ginseng is perceived as safe owing to its natural origin, extensive historical uses, and accumulated scientific clinical studies in humans. According to oriental medicine theory, <em>Panax ginseng</em> is categorized as having warm properties, while <em>Panax quinquefolium</em>, called American ginseng, is classified as having cool properties. Based on this, it is said that <em>Panax ginseng</em> might cause an elevation of body temperature, such as sensations of warmth or heat, whereas <em>Panax quinquefolium</em> provides cooling effects. However, scientific evidence for comparing these parallel thermogenic effects of two species is scarce. This focused review summarizes clinical trials and animal studies regarding the heat responses of two Panax species. This review aims to provide an overview of current scientific data on the thermogenic effects inducing a heat sensation and a hot feeling of Korean ginseng and American ginseng.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 389-394"},"PeriodicalIF":6.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307199","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 : 2025-07-01Epub Date: 2025-03-25DOI: 10.1016/j.jgr.2025.03.009
Yu-Xin Zhang , Hui Wan , Guan-Yue Shan , Jun-Ya Cheng , Zhi-Cheng Gao , Yi-Ying Liu , Wen-Na Shi , Zi-Jun Sun , Hai-Jun Li
Background
Hyperuricemia nephropathy (HN) is a form of renal injury caused by hyperuricemia, which can progress to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Ginsenoside Rg5, a major bioactive compound isolated from Panax ginseng, is recognized for its notable effects, including anti-inflammatory, antioxidant, and anticancer activities.
Method
The toxic doses of MSU crystals and Rg5-induced HK-2 cell damage were assessed using the CCK-8 assay and quantifying oxidative stress markers (MDA, GSH, SOD). Intracellular stress was evaluated with JC-1 and DCFH-DA probes. Bioinformatics analysis identified NOX1, TLR4, and Bcl-2 as potential targets. The protein expression associated with stress, inflammation, pyroptosis, and apoptosis in HK-2 cells was evaluated through a combination of Western blotting, ELISA, flow cytometry, immunofluorescence, and overexpression methods. An HN mice model was established through administration of YE and adenine, and the effects of Rg5 were evaluated. The in vivo mechanisms were further verified.
Results
Rg5 reduced serum uric acid, BUN, ADH, and creatinine levels in MSU crystals-stimulated HK-2 cells and hyperuricemic mice, alleviating renal damage. Rg5 inhibited NOX1 and suppressed the TLR4 pathway, reducing oxidative stress, inflammation, pyroptosis, and apoptosis. NOX1 overexpression reversed the effects of Rg5, while TLR4 overexpression had no effect. Rg5's efficacy was similar to NOX1 inhibitor ML171.
Conclusion
These results indicate that Rg5 can modulate the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating oxidative stress, inflammation, pyroptosis, and apoptosis in HN, highlighting its potential as a therapeutic approach for controlling HN.
{"title":"Ginsenoside Rg5 modulates the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating inflammation, apoptosis and pyroptosis in hyperuricemia nephropathy","authors":"Yu-Xin Zhang , Hui Wan , Guan-Yue Shan , Jun-Ya Cheng , Zhi-Cheng Gao , Yi-Ying Liu , Wen-Na Shi , Zi-Jun Sun , Hai-Jun Li","doi":"10.1016/j.jgr.2025.03.009","DOIUrl":"10.1016/j.jgr.2025.03.009","url":null,"abstract":"<div><h3>Background</h3><div>Hyperuricemia nephropathy (HN) is a form of renal injury caused by hyperuricemia, which can progress to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Ginsenoside Rg5, a major bioactive compound isolated from Panax ginseng, is recognized for its notable effects, including anti-inflammatory, antioxidant, and anticancer activities.</div></div><div><h3>Method</h3><div>The toxic doses of MSU crystals and Rg5-induced HK-2 cell damage were assessed using the CCK-8 assay and quantifying oxidative stress markers (MDA, GSH, SOD). Intracellular stress was evaluated with JC-1 and DCFH-DA probes. Bioinformatics analysis identified NOX1, TLR4, and Bcl-2 as potential targets. The protein expression associated with stress, inflammation, pyroptosis, and apoptosis in HK-2 cells was evaluated through a combination of Western blotting, ELISA, flow cytometry, immunofluorescence, and overexpression methods. An HN mice model was established through administration of YE and adenine, and the effects of Rg5 were evaluated. The in vivo mechanisms were further verified.</div></div><div><h3>Results</h3><div>Rg5 reduced serum uric acid, BUN, ADH, and creatinine levels in MSU crystals-stimulated HK-2 cells and hyperuricemic mice, alleviating renal damage. Rg5 inhibited NOX1 and suppressed the TLR4 pathway, reducing oxidative stress, inflammation, pyroptosis, and apoptosis. NOX1 overexpression reversed the effects of Rg5, while TLR4 overexpression had no effect. Rg5's efficacy was similar to NOX1 inhibitor ML171.</div></div><div><h3>Conclusion</h3><div>These results indicate that Rg5 can modulate the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating oxidative stress, inflammation, pyroptosis, and apoptosis in HN, highlighting its potential as a therapeutic approach for controlling HN.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 426-437"},"PeriodicalIF":6.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307212","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 : 2025-07-01Epub Date: 2025-04-04DOI: 10.1016/j.jgr.2025.03.010
Jung Ho Hwang , Se Yong Park , Ju-Hee Kang , Hyun Jin Jung , Jiwon Park , Han-Joo Maeng , Min-Koo Choi , Ha Suk Song , Im-Sook Song , Seung Hyun Oh
Background
Despite the efficacy of anticancer drugs, patients frequently experience relapse, metastasis, and resistance. A promising therapeutic approach not only targets cancer cell growth but also modulates cancer-associated fibroblasts, which support malignancies. Compound K (CK), a metabolite derived from red ginseng, has demonstrated anticancer properties. Recently, we developed a CK-enriched red ginseng extract (CKP) and explored its potential to suppress lung cancer by inhibiting cancer cell proliferation and inactivating fibroblasts.
Methods
To evaluate the in vitro efficacy of CKP in inhibiting lung cancer cell proliferation, MTT and colony formation assays were performed. The apoptotic effects of CKP on lung cancer cells were assessed using Western blot and flow cytometry. Furthermore, the ability of CKP to inhibit TGF β1-induced migration of cancer cells was investigated through Western blot, RT-PCR, and a wound healing assay. Additionally, the impact of CKP on lung fibroblast inactivation was examined via Western blot and RT-PCR analysis. For in vivo experiments, a xenograft model was utilized, incorporating a combination of lung cancer cells and lung fibroblasts in xenografts.
Results
CKP significantly reduced the proliferation and invasiveness of TGF-β1-stimulated A549 cells, demonstrating its potential to inactivate lung fibroblasts. Additionally, CKP inhibited the secretion of cytokines, such as interleukin-6, interleukin-8, and TGF-β1, by activated fibroblasts. In vivo, CKP markedly inhibited tumor growth in the xenograft model.
Conclusion
In conclusion, CKP effectively induced apoptosis in lung cancer cells, suppressed metastasis, and inactivated fibroblasts, thereby preventing cancer invasion and reducing extracellular matrix production, highlighting its potential as a novel anticancer agent.
{"title":"Compound K-enriched Korean red ginseng prevents lung cancer progression by targeting cancer cells and fibroblasts","authors":"Jung Ho Hwang , Se Yong Park , Ju-Hee Kang , Hyun Jin Jung , Jiwon Park , Han-Joo Maeng , Min-Koo Choi , Ha Suk Song , Im-Sook Song , Seung Hyun Oh","doi":"10.1016/j.jgr.2025.03.010","DOIUrl":"10.1016/j.jgr.2025.03.010","url":null,"abstract":"<div><h3>Background</h3><div>Despite the efficacy of anticancer drugs, patients frequently experience relapse, metastasis, and resistance. A promising therapeutic approach not only targets cancer cell growth but also modulates cancer-associated fibroblasts, which support malignancies. Compound K (CK), a metabolite derived from red ginseng, has demonstrated anticancer properties. Recently, we developed a CK-enriched red ginseng extract (CKP) and explored its potential to suppress lung cancer by inhibiting cancer cell proliferation and inactivating fibroblasts.</div></div><div><h3>Methods</h3><div>To evaluate the <em>in vitro</em> efficacy of CKP in inhibiting lung cancer cell proliferation, MTT and colony formation assays were performed. The apoptotic effects of CKP on lung cancer cells were assessed using Western blot and flow cytometry. Furthermore, the ability of CKP to inhibit TGF β1-induced migration of cancer cells was investigated through Western blot, RT-PCR, and a wound healing assay. Additionally, the impact of CKP on lung fibroblast inactivation was examined via Western blot and RT-PCR analysis. For <em>in vivo</em> experiments, a xenograft model was utilized, incorporating a combination of lung cancer cells and lung fibroblasts in xenografts.</div></div><div><h3>Results</h3><div>CKP significantly reduced the proliferation and invasiveness of TGF-β1-stimulated A549 cells, demonstrating its potential to inactivate lung fibroblasts. Additionally, CKP inhibited the secretion of cytokines, such as interleukin-6, interleukin-8, and TGF-β1, by activated fibroblasts. <em>In vivo</em>, CKP markedly inhibited tumor growth in the xenograft model.</div></div><div><h3>Conclusion</h3><div>In conclusion, CKP effectively induced apoptosis in lung cancer cells, suppressed metastasis, and inactivated fibroblasts, thereby preventing cancer invasion and reducing extracellular matrix production, highlighting its potential as a novel anticancer agent.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 438-450"},"PeriodicalIF":6.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307213","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 : 2025-07-01Epub Date: 2025-04-10DOI: 10.1016/j.jgr.2025.04.002
Abdul Wahab Akram , Jung-Hae Shin , Uyanga Batmunkh , Evelyn Saba , Yong-Myung Kang , Sunjun Jung , Jee Eun Han , Sung Dae Kim , Dongmi Kwak , Hyuk-woo Kwon , Man Hee Rhee
Background
Platelet hyperactivation is a major factor in thrombotic complications such as myocardial infarction and ischemic stroke. Ginsenoside Rg5 is a minor ginsenoside, and among its various beneficial pharmacological effects, its antithrombotic potential has not been extensively studied.
Methods
Human platelets were isolated and treated with Rg5 (35-100 μM) before stimulation with agonists such as collagen, thrombin, and U46619. Platelet aggregation, granule secretion, calcium mobilization, thromboxane A2 production, fibrinogen binding, and clot retraction were evaluated. The effects of Rg5 on signaling pathways were determined via Western blot analysis of key proteins. In vivo, the antithrombotic efficacy was assessed using ferric chloride (FeCl3)-induced thrombosis in mice.
Results
Rg5 dose-dependently inhibited collagen-induced platelet aggregation (IC50 = 42.5 μM) and selectively inhibited GPVI-mediated signaling compared to thrombin and U46619. Rg5 suppressed intracellular calcium mobilization, granule secretion, and thromboxane A2 production, with no cytotoxicity observed. Rg5 downregulated key signaling proteins (p-PI3K, p-AKT, p-cPLA2, and p-p38) while upregulating p-VASP (S157 and S239), suggesting its role in elevating cyclic nucleotide signaling. Additionally, Rg5 inhibited CD162 expression that was induced in the presence of collagen and oxidized low-density lipoprotein. It also prevented fibrinogen and fibronectin binding and significantly reduced clot retraction. In vivo, Rg5 (20 mg/kg) significantly prolonged the carotid artery occlusion time and prevented thrombus formation, outperforming aspirin (100 mg/kg).
Conclusion
Ginsenoside Rg5 exhibits potent antiplatelet activity by selectively targeting GPVI-mediated platelet activation and modulating key intracellular signaling pathways. These results suggest that Rg5 could be utilized to develop safer and natural antiplatelet therapies.
{"title":"Ginsenoside Rg5 inhibits platelet aggregation by regulating GPVI signaling pathways and ferric chloride-induced thrombosis","authors":"Abdul Wahab Akram , Jung-Hae Shin , Uyanga Batmunkh , Evelyn Saba , Yong-Myung Kang , Sunjun Jung , Jee Eun Han , Sung Dae Kim , Dongmi Kwak , Hyuk-woo Kwon , Man Hee Rhee","doi":"10.1016/j.jgr.2025.04.002","DOIUrl":"10.1016/j.jgr.2025.04.002","url":null,"abstract":"<div><h3>Background</h3><div>Platelet hyperactivation is a major factor in thrombotic complications such as myocardial infarction and ischemic stroke. Ginsenoside Rg5 is a minor ginsenoside, and among its various beneficial pharmacological effects, its antithrombotic potential has not been extensively studied.</div></div><div><h3>Methods</h3><div>Human platelets were isolated and treated with Rg5 (35-100 μM) before stimulation with agonists such as collagen, thrombin, and U46619. Platelet aggregation, granule secretion, calcium mobilization, thromboxane A<sub>2</sub> production, fibrinogen binding, and clot retraction were evaluated. The effects of Rg5 on signaling pathways were determined via Western blot analysis of key proteins. <em>In vivo</em>, the antithrombotic efficacy was assessed using ferric chloride (FeCl<sub>3</sub>)-induced thrombosis in mice.</div></div><div><h3>Results</h3><div>Rg5 dose-dependently inhibited collagen-induced platelet aggregation (IC<sub>50</sub> = 42.5 μM) and selectively inhibited GPVI-mediated signaling compared to thrombin and U46619. Rg5 suppressed intracellular calcium mobilization, granule secretion, and thromboxane A<sub>2</sub> production, with no cytotoxicity observed. Rg5 downregulated key signaling proteins (p-PI3K, p-AKT, p-cPLA2, and p-p38) while upregulating p-VASP (S157 and S239), suggesting its role in elevating cyclic nucleotide signaling. Additionally, Rg5 inhibited CD162 expression that was induced in the presence of collagen and oxidized low-density lipoprotein. It also prevented fibrinogen and fibronectin binding and significantly reduced clot retraction. <em>In vivo</em>, Rg5 (20 mg/kg) significantly prolonged the carotid artery occlusion time and prevented thrombus formation, outperforming aspirin (100 mg/kg).</div></div><div><h3>Conclusion</h3><div>Ginsenoside Rg5 exhibits potent antiplatelet activity by selectively targeting GPVI-mediated platelet activation and modulating key intracellular signaling pathways. These results suggest that Rg5 could be utilized to develop safer and natural antiplatelet therapies.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 460-469"},"PeriodicalIF":6.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307215","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 : 2025-05-01Epub Date: 2025-02-10DOI: 10.1016/j.jgr.2025.02.001
Ji Zhang , Jing Xie , Zhiqiang Niu , Long You , Yanan Liu , Rui Guo , Guigui Yang , Ziliang He , Ting Shen , Honggang Wang , Qi Yan , Weicheng Hu
Background
Ginsenoside Rg2 (G-Rg2), a major active compound of Panax ginseng, exhibits a wide range of pharmacological properties, including anticancer, antioxidant and neuroprotective effects. However, the mechanisms by which G-Rg2 mitigates ulcerative colitis (UC) have not been clearly elucidated.
Aims
In the present study, we aimed to elucidate the underlying mechanisms by which G-Rg2 mitigated UC.
Methods
In this study, we investigated the efficacy of G-Rg2 in ameliorating dextran sulfate sodium (DSS)-induced UC and its potential mechanisms using a DSS-induced UC mouse model and Lipopolysaccharides (LPS)/nigericin (Nig)-induced NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation on immortalized bone marrow-derived macrophages (iBMDMs).
Results
Oral administration of G-Rg2 at doses of 10 and 20 mg/kg significantly mitigated weight loss, normalized food and water intake, and improved colon histopathology in DSS-induced UC mice. G-Rg2 also restored mRNA expression levels of occludin, claudin-3, zona occluden (ZO)-1 and mucin 2, thereby enhancing intestinal barrier integrity. G-Rg2 significantly suppressed the nuclear translocation of p65, the subunit of nuclear factor kappa-B (NF-κB), as well as downregulated NLRP3, cleaved IL-1β and caspase1 p20 expression induced by LPS/Nig in iBMDMs.
Conclusion
G-Rg2 effectively reduced colon inflammation in DSS-induced UC mice and diminishes inflammatory responses under LPS/Nig conditions by regulating NF-κB/NLRP3 pathway, thereby inhibiting NLRP3 inflammasome activation, which may serve as a potent therapeutic agent for UC.
{"title":"Ginsenoside Rg2, a principal effective ingredient of Panax ginseng, attenuates DSS-induced ulcerative colitis through NF-κB/NLRP3 pathway","authors":"Ji Zhang , Jing Xie , Zhiqiang Niu , Long You , Yanan Liu , Rui Guo , Guigui Yang , Ziliang He , Ting Shen , Honggang Wang , Qi Yan , Weicheng Hu","doi":"10.1016/j.jgr.2025.02.001","DOIUrl":"10.1016/j.jgr.2025.02.001","url":null,"abstract":"<div><h3>Background</h3><div>Ginsenoside Rg2 (G-Rg2), a major active compound of <em>Panax ginseng</em>, exhibits a wide range of pharmacological properties, including anticancer, antioxidant and neuroprotective effects. However, the mechanisms by which G-Rg2 mitigates ulcerative colitis (UC) have not been clearly elucidated.</div></div><div><h3>Aims</h3><div>In the present study, we aimed to elucidate the underlying mechanisms by which G-Rg2 mitigated UC.</div></div><div><h3>Methods</h3><div>In this study, we investigated the efficacy of G-Rg2 in ameliorating dextran sulfate sodium (DSS)-induced UC and its potential mechanisms using a DSS-induced UC mouse model and Lipopolysaccharides (LPS)/nigericin (Nig)-induced NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation on immortalized bone marrow-derived macrophages (iBMDMs).</div></div><div><h3>Results</h3><div>Oral administration of G-Rg2 at doses of 10 and 20 mg/kg significantly mitigated weight loss, normalized food and water intake, and improved colon histopathology in DSS-induced UC mice. G-Rg2 also restored mRNA expression levels of occludin, claudin-3, zona occluden (ZO)-1 and mucin 2, thereby enhancing intestinal barrier integrity. G-Rg2 significantly suppressed the nuclear translocation of p65, the subunit of nuclear factor kappa-B (NF-κB), as well as downregulated NLRP3, cleaved IL-1β and caspase1 p20 expression induced by LPS/Nig in iBMDMs.</div></div><div><h3>Conclusion</h3><div>G-Rg2 effectively reduced colon inflammation in DSS-induced UC mice and diminishes inflammatory responses under LPS/Nig conditions by regulating NF-κB/NLRP3 pathway, thereby inhibiting NLRP3 inflammasome activation, which may serve as a potent therapeutic agent for UC.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 282-293"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870183","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 : 2025-05-01Epub Date: 2025-03-20DOI: 10.1016/j.jgr.2025.03.006
Ye Zhang , Saisai Ma , Yichen Xu , Shuaida Wu , Shuangshuang Wu , Minmin Liu , Yingjie Guo , Yang Zhan
Background
Panax ginseng Meyer is a well-known herb in traditional Chinese medicine, with ginsenosides being its primary bioactive components. Among these, 20(S)-protopanaxadiol (20(S)-PPD) has demonstrated anti-tumor effects in various cancers. However, its role in acute myeloid leukemia (AML) remains unclear.
Methods
MTT assays were conducted to assess the impact of 20(S)-PPD on AML cell proliferation, while flow cytometry was used to analyze its effects on apoptosis. Western blotting and network pharmacology analyses were employed to explore the signaling pathways and protein expression levels modulated by 20(S)-PPD in AML. c-Myc mRNA levels in AML cells were quantified using RT-PCR.
Results
20(S)-PPD effectively inhibits proliferation and induces apoptosis in AML cells, both in vitro and in patient samples. It achieves this by inhibiting the PI3K/AKT/mTOR pathway and activating the PERK/ATF4/CHOP pathway. Additionally, 20(S)-PPD reduces c-Myc protein and mRNA levels, primarily by decreasing c-Myc mRNA stability. Moreover, combining 20(S)-PPD with ABT-199 significantly enhances pro-apoptotic effects and markedly reduces c-Myc protein and mRNA levels in both AML and cytarabine-resistant (AraC-R) AML cells. This combination therapy holds promise for overcoming resistance and improving treatment outcomes in AML.
Conclusion
This study demonstrates the potent antitumor activity of 20(S)-PPD in AML and elucidates its underlying mechanisms. Notably, 20(S)-PPD exhibits significant antitumor effects against AML cells, both as a single agent and in combination with ABT-199, where it displays pronounced synergy. These results suggest a promising new therapeutic strategy for AML treatment.
{"title":"The antitumor effects and apoptotic mechanism of 20(S)-Protopanaxadiol in acute myeloid leukemia","authors":"Ye Zhang , Saisai Ma , Yichen Xu , Shuaida Wu , Shuangshuang Wu , Minmin Liu , Yingjie Guo , Yang Zhan","doi":"10.1016/j.jgr.2025.03.006","DOIUrl":"10.1016/j.jgr.2025.03.006","url":null,"abstract":"<div><h3>Background</h3><div>Panax ginseng Meyer is a well-known herb in traditional Chinese medicine, with ginsenosides being its primary bioactive components. Among these, 20(S)-protopanaxadiol (20(S)-PPD) has demonstrated anti-tumor effects in various cancers. However, its role in acute myeloid leukemia (AML) remains unclear.</div></div><div><h3>Methods</h3><div>MTT assays were conducted to assess the impact of 20(S)-PPD on AML cell proliferation, while flow cytometry was used to analyze its effects on apoptosis. Western blotting and network pharmacology analyses were employed to explore the signaling pathways and protein expression levels modulated by 20(S)-PPD in AML. c-Myc mRNA levels in AML cells were quantified using RT-PCR.</div></div><div><h3>Results</h3><div>20(S)-PPD effectively inhibits proliferation and induces apoptosis in AML cells, both in vitro and in patient samples. It achieves this by inhibiting the PI3K/AKT/mTOR pathway and activating the PERK/ATF4/CHOP pathway. Additionally, 20(S)-PPD reduces c-Myc protein and mRNA levels, primarily by decreasing c-Myc mRNA stability. Moreover, combining 20(S)-PPD with ABT-199 significantly enhances pro-apoptotic effects and markedly reduces c-Myc protein and mRNA levels in both AML and cytarabine-resistant (AraC-R) AML cells. This combination therapy holds promise for overcoming resistance and improving treatment outcomes in AML.</div></div><div><h3>Conclusion</h3><div>This study demonstrates the potent antitumor activity of 20(S)-PPD in AML and elucidates its underlying mechanisms. Notably, 20(S)-PPD exhibits significant antitumor effects against AML cells, both as a single agent and in combination with ABT-199, where it displays pronounced synergy. These results suggest a promising new therapeutic strategy for AML treatment.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 306-314"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870185","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 : 2025-05-01Epub Date: 2025-01-01DOI: 10.1016/j.jgr.2024.12.007
Jaewook Kim , Bae Young Choi , Donghwan Shim , Ick-Hyun Jo
Background
Panax ginseng fruit tissue is one of the richest sources of valuable constituents such as ginsenosides and anthocyanins. Although anthocyanins extracted from the fruit tissue of P. ginseng are utilized, it is uncertain how anthocyanin accumulation is regulated and which anthocyanin varieties are synthesized.
Methods
Fruits of four P. ginseng cultivars were collected for total RNA extraction and RNA-Seq analysis using the Illumina HiSeq X platform. Anthocyanins were extracted and analyzed by UPLC-DAD-QToF/MS to identify and quantify individual derivatives. Differentially expressed genes (DEGs) were identified, followed by functional annotation and network analysis to evaluate gene expression patterns.
Results
Comparative transcriptome analysis of four differently colored P. ginseng cultivars revealed that flavonoid biosynthetic genes associated with the karrikin response and jasmonate-responsive genes were upregulated in anthocyanin-rich fruits. Network analysis further revealed a putative regulatory complex consists of karrikin- and jasmonate-responsive genes along with flavonoid biosynthetic genes. Analyzing the UPLC-DAD extracts of the fruit of cv. Chunpoong found that the fruit tissue of P. ginseng is rich in pelargonidin.
Conclusion
Our research provides how anthocyanin is accumulated and which type is accumulated in fruit tissue of P. ginseng, including the original compound, pelargonidin 3-O-(2″-O-glucosyl)galactoside. We expect that our research will lead to improved breeding efficiency for the development of cultivars containing more flavonoid species that are beneficial to humans.
人参果实组织是人参皂苷和花青素等有价值成分最丰富的来源之一。虽然利用了从人参果实组织中提取的花青素，但花青素的积累是如何调控的以及哪些花青素品种是合成的还不清楚。方法采集4个人参品种的果实，采用Illumina HiSeq X平台进行总RNA提取和RNA- seq分析。提取花青素，采用UPLC-DAD-QToF/MS进行分析，对单个衍生物进行鉴定和定量。鉴定差异表达基因（deg），然后通过功能注释和网络分析来评估基因表达模式。结果4个不同颜色人参品种的转录组对比分析显示，花青素丰富的果实中，与卡里金反应相关的类黄酮生物合成基因和茉莉素反应相关的基因均上调。网络分析进一步揭示了一个假设的调控复合体，由卡瑞金和茉莉酸响应基因以及类黄酮生物合成基因组成。枸杞子UPLC-DAD提取物的分析。春蓬发现，人参果实组织中含有丰富的天竺葵苷。结论本研究揭示了花青素在人参果实组织中积累的途径和类型，包括其原始化合物花青素3-O-（2″- o -葡萄糖基）半乳糖苷。我们期望我们的研究将有助于提高育种效率，开发含有更多对人类有益的黄酮类化合物的品种。
{"title":"Complex transcriptome network regulates the anthocyanin accumulation of four Panax ginseng cultivars in fruit","authors":"Jaewook Kim , Bae Young Choi , Donghwan Shim , Ick-Hyun Jo","doi":"10.1016/j.jgr.2024.12.007","DOIUrl":"10.1016/j.jgr.2024.12.007","url":null,"abstract":"<div><h3>Background</h3><div><em>Panax ginseng</em> fruit tissue is one of the richest sources of valuable constituents such as ginsenosides and anthocyanins. Although anthocyanins extracted from the fruit tissue of <em>P. ginseng</em> are utilized, it is uncertain how anthocyanin accumulation is regulated and which anthocyanin varieties are synthesized.</div></div><div><h3>Methods</h3><div>Fruits of four <em>P. ginseng</em> cultivars were collected for total RNA extraction and RNA-Seq analysis using the Illumina HiSeq X platform. Anthocyanins were extracted and analyzed by UPLC-DAD-QToF/MS to identify and quantify individual derivatives. Differentially expressed genes (DEGs) were identified, followed by functional annotation and network analysis to evaluate gene expression patterns.</div></div><div><h3>Results</h3><div>Comparative transcriptome analysis of four differently colored <em>P. ginseng</em> cultivars revealed that flavonoid biosynthetic genes associated with the karrikin response and jasmonate-responsive genes were upregulated in anthocyanin-rich fruits. Network analysis further revealed a putative regulatory complex consists of karrikin- and jasmonate-responsive genes along with flavonoid biosynthetic genes. Analyzing the UPLC-DAD extracts of the fruit of cv. Chunpoong found that the fruit tissue of <em>P. ginseng</em> is rich in pelargonidin.</div></div><div><h3>Conclusion</h3><div>Our research provides how anthocyanin is accumulated and which type is accumulated in fruit tissue of <em>P. ginseng,</em> including the original compound, pelargonidin 3-O-(2″-O-glucosyl)galactoside. We expect that our research will lead to improved breeding efficiency for the development of cultivars containing more flavonoid species that are beneficial to humans.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 315-325"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870382","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 : 2025-05-01Epub Date: 2025-01-27DOI: 10.1016/j.jgr.2025.01.004
Churong Li , Biao Zhao , Jing Xiong , Linjie Li , Dalong Pang , Keith Unger , Mira Jung , Jiahua Lyu , Hao Kuang , Long Liang , Tao Li , Long Chen , Hansong Bai
Background
Ginsenoside Rg5 possesses potent anti-oxidative, anti-inflammatory, and cytoprotective properties. This study explored the protective effects of ginsenoside Rg5 on radiation-induced pulmonary microvascular endothelial cells (PMECs) injury and the associated molecular mechanisms.
Materials and methods
C57BL/6 mice were used for in vivo studies and primary human PMECs (PPMECs) were utilized as in vitro models. Mice with or without ginsenoside Rg5 pretreatment were irradiated by varying doses. Lung tissues were analyzed for histopathological changes and the expression of endothelial markers. In vitro, PPMECs were irradiated with or without ginsenoside Rg5 pretreatment and analyzed for apoptosis, oxidative stress, mitochondrial function, and endothelial barrier integrity.
Results
Ginsenoside Rg5 pretreatment attenuated radiation-induced acute lung damage, preserved endothelial cell junction integrity, and maintained endothelial barrier function in vivo. In vitro, ginsenoside Rg5 significantly reduced IR-induced oxidative stress, apoptosis, and mitochondrial dysfunction in PPMECs. Ginsenoside Rg5 suppressed radiation-induced Mfn2 acetylation and proteasomal degradation via Sirt1-mediated deacetylation, thereby preserving mitochondrial dynamics and integrity. The protective effects of ginsenoside Rg5 on the integrity of mitochondrial and endothelial tight junction proteins and barrier function were also Sirt1-dependent.
Conclusions
Ginsenoside Rg5 exerts a protective effect against radiation-induced endothelial injury by modulating mitochondrial dynamics and function, as well as maintaining endothelial barrier integrity, in a Sirt1-dependent manner.
{"title":"Ginsenoside Rg5 alleviates radiation-induced acute lung vascular endothelium injury by reducing mitochondrial apoptosis via Sirt1","authors":"Churong Li , Biao Zhao , Jing Xiong , Linjie Li , Dalong Pang , Keith Unger , Mira Jung , Jiahua Lyu , Hao Kuang , Long Liang , Tao Li , Long Chen , Hansong Bai","doi":"10.1016/j.jgr.2025.01.004","DOIUrl":"10.1016/j.jgr.2025.01.004","url":null,"abstract":"<div><h3>Background</h3><div>Ginsenoside Rg5 possesses potent anti-oxidative, anti-inflammatory, and cytoprotective properties. This study explored the protective effects of ginsenoside Rg5 on radiation-induced pulmonary microvascular endothelial cells (PMECs) injury and the associated molecular mechanisms.</div></div><div><h3>Materials and methods</h3><div>C57BL/6 mice were used for <em>in vivo</em> studies and primary human PMECs (PPMECs) were utilized as <em>in vitro</em> models. Mice with or without ginsenoside Rg5 pretreatment were irradiated by varying doses. Lung tissues were analyzed for histopathological changes and the expression of endothelial markers. <em>In vitro</em>, PPMECs were irradiated with or without ginsenoside Rg5 pretreatment and analyzed for apoptosis, oxidative stress, mitochondrial function, and endothelial barrier integrity.</div></div><div><h3>Results</h3><div>Ginsenoside Rg5 pretreatment attenuated radiation-induced acute lung damage, preserved endothelial cell junction integrity, and maintained endothelial barrier function <em>in vivo</em>. <em>In vitro</em>, ginsenoside Rg5 significantly reduced IR-induced oxidative stress, apoptosis, and mitochondrial dysfunction in PPMECs. Ginsenoside Rg5 suppressed radiation-induced Mfn2 acetylation and proteasomal degradation via Sirt1-mediated deacetylation, thereby preserving mitochondrial dynamics and integrity. The protective effects of ginsenoside Rg5 on the integrity of mitochondrial and endothelial tight junction proteins and barrier function were also Sirt1-dependent.</div></div><div><h3>Conclusions</h3><div>Ginsenoside Rg5 exerts a protective effect against radiation-induced endothelial injury by modulating mitochondrial dynamics and function, as well as maintaining endothelial barrier integrity, in a Sirt1-dependent manner.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 260-270"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870508","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 : 2025-05-01Epub Date: 2025-03-21DOI: 10.1016/j.jgr.2025.03.004
A Young Kim, Ji-Yong Jung, Donghyun Kim, Jeong Hun Cho, Yong Deog Hong, Hyoung-June Kim, Si-Young Cho
We evaluated the anti-accelerated epidermal skin aging effects of compound K (CK) on keratinocytes using IL-17A and ultraviolet B. CK restored epidermal functions and reduced the induction of pro-inflammatory cytokines by inhibiting NF-κB and p38 MAPK activation. CK plays a significant role in controlling accelerated epidermal skin aging.
{"title":"Compound K suppresses epidermal aging induced by IL-17A treatment and UVB irradiation","authors":"A Young Kim, Ji-Yong Jung, Donghyun Kim, Jeong Hun Cho, Yong Deog Hong, Hyoung-June Kim, Si-Young Cho","doi":"10.1016/j.jgr.2025.03.004","DOIUrl":"10.1016/j.jgr.2025.03.004","url":null,"abstract":"<div><div>We evaluated the anti-accelerated epidermal skin aging effects of compound K (CK) on keratinocytes using IL-17A and ultraviolet B. CK restored epidermal functions and reduced the induction of pro-inflammatory cytokines by inhibiting NF-κB and p38 MAPK activation. CK plays a significant role in controlling accelerated epidermal skin aging.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 326-330"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870503","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 : 2025-05-01Epub Date: 2024-12-06DOI: 10.1016/j.jgr.2024.12.003
Yeong-Geun Lee , Woojae Hong , Young Mi Cho , Jeong Eun Kwon , Deok-Chun Yang , Hyunggun Kim , Se Chan Kang
Background
Chronic fatigue deleteriously affects the quality of life, thereby impairing physical and social functions and subsequently leading to financial and social problems. This study investigated the anti-fatigue effects of Korean Red Ginseng (KRG) extract in healthy middle-aged Japanese adults.
Methods
Forty-six participants were randomly divided into two groups (KRG and placebo). KRG (960 mg) or placebo capsules were administered for 3 weeks. The effect of KRG on fatigue was evaluated using visual analogue scale (VAS), plasma lactic acid, and cortisol levels.
Results and conclusions
Three-week consumption of KRG extract resulted in a significant decrease in the fatigue VAS score compared to the placebo group (p = 0.035). No significant difference was found in plasma cortisol and lactic acid levels between the groups. There were no differences between groups in the incidence of adverse events and the results of urinalysis, hematology, and biochemistry. These findings suggest the potential of KRG extract in mitigating fatigue and the safety of KRG extracts in healthy adults.
{"title":"Anti-fatigue effects of Korean Red Ginseng extract in healthy Japanese adults: A randomized, double-blind, placebo-controlled study","authors":"Yeong-Geun Lee , Woojae Hong , Young Mi Cho , Jeong Eun Kwon , Deok-Chun Yang , Hyunggun Kim , Se Chan Kang","doi":"10.1016/j.jgr.2024.12.003","DOIUrl":"10.1016/j.jgr.2024.12.003","url":null,"abstract":"<div><h3>Background</h3><div>Chronic fatigue deleteriously affects the quality of life, thereby impairing physical and social functions and subsequently leading to financial and social problems. This study investigated the anti-fatigue effects of Korean Red Ginseng (KRG) extract in healthy middle-aged Japanese adults.</div></div><div><h3>Methods</h3><div>Forty-six participants were randomly divided into two groups (KRG and placebo). KRG (960 mg) or placebo capsules were administered for 3 weeks. The effect of KRG on fatigue was evaluated using visual analogue scale (VAS), plasma lactic acid, and cortisol levels.</div></div><div><h3>Results and conclusions</h3><div>Three-week consumption of KRG extract resulted in a significant decrease in the fatigue VAS score compared to the placebo group (p = 0.035). No significant difference was found in plasma cortisol and lactic acid levels between the groups. There were no differences between groups in the incidence of adverse events and the results of urinalysis, hematology, and biochemistry. These findings suggest the potential of KRG extract in mitigating fatigue and the safety of KRG extracts in healthy adults.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 237-247"},"PeriodicalIF":6.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870506","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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