Pub Date : 2025-09-01Epub Date: 2025-04-12DOI: 10.1016/j.jgr.2025.04.003
Joongyu Kang, Jin Ho Choi, Sang Hyub Lee, Junyeol Kim, Tae Seung Lee, Sung Hoon Chang, Yong Soo Song, In Rae Cho, Woo Hyun Paik, Ji Kon Ryu
Background: Managing symptoms of chronic pancreatitis (CP) remains a significant challenge. Korean Red ginseng (KRG), a well-known herbal supplement, has shown potential benefits in various health conditions, prompting its investigation in CP patients.
Methods: We conducted a single-arm, prospective clinical trial to evaluate the effect of KRG on quality of life in CP patients exhibiting mild symptoms, as defined by a Clinical Global Impression (CGI) score of 0 or 1. 40 patients were enrolled and assessed at baseline, as well as at 30, 90, and 180 days. The primary outcome was an improvement in CGI scores, with secondary outcomes including changes in Pancreatic Exocrine Insufficiency Questionnaire (PEI-Q) scores.
Results: A total of 40 patients were enrolled in this study, and 39 participants were analyzed. Results showed significant improvements in CGI scores at all examined intervals (days 0-30, 0-90, 0-180; p < 0.05). The PEI-Q score also significantly improved from day 0 to day 180 (p < 0.05). Two adverse events (AEs) probably related to KRG were reported, and all AEs were improved with conservative managements.
Conclusion: KRG supplementation significantly improves quality of life in CP patients with mild symptoms. These findings suggest that KRG may be a beneficial adjunct therapy in this patient population. Further research is needed to explore KRG's pharmacological mechanisms, its use in combination with other treatments, and its effects in patients with more severe symptoms. (CRIS number: KCT0009681).
{"title":"Korean Red ginseng supplements improve quality of life in patients with mild chronic pancreatitis symptoms: A prospective clinical trial.","authors":"Joongyu Kang, Jin Ho Choi, Sang Hyub Lee, Junyeol Kim, Tae Seung Lee, Sung Hoon Chang, Yong Soo Song, In Rae Cho, Woo Hyun Paik, Ji Kon Ryu","doi":"10.1016/j.jgr.2025.04.003","DOIUrl":"10.1016/j.jgr.2025.04.003","url":null,"abstract":"<p><strong>Background: </strong>Managing symptoms of chronic pancreatitis (CP) remains a significant challenge. Korean Red ginseng (KRG), a well-known herbal supplement, has shown potential benefits in various health conditions, prompting its investigation in CP patients.</p><p><strong>Methods: </strong>We conducted a single-arm, prospective clinical trial to evaluate the effect of KRG on quality of life in CP patients exhibiting mild symptoms, as defined by a Clinical Global Impression (CGI) score of 0 or 1. 40 patients were enrolled and assessed at baseline, as well as at 30, 90, and 180 days. The primary outcome was an improvement in CGI scores, with secondary outcomes including changes in Pancreatic Exocrine Insufficiency Questionnaire (PEI-Q) scores.</p><p><strong>Results: </strong>A total of 40 patients were enrolled in this study, and 39 participants were analyzed. Results showed significant improvements in CGI scores at all examined intervals (days 0-30, 0-90, 0-180; p < 0.05). The PEI-Q score also significantly improved from day 0 to day 180 (p < 0.05). Two adverse events (AEs) probably related to KRG were reported, and all AEs were improved with conservative managements.</p><p><strong>Conclusion: </strong>KRG supplementation significantly improves quality of life in CP patients with mild symptoms. These findings suggest that KRG may be a beneficial adjunct therapy in this patient population. Further research is needed to explore KRG's pharmacological mechanisms, its use in combination with other treatments, and its effects in patients with more severe symptoms. (CRIS number: KCT0009681).</p>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 5","pages":"502-508"},"PeriodicalIF":5.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144956816","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}
Background: Myocardial hypertrophy is a crucial pathological change that occurs during post-anthracycline treatment cardiomyopathy. The effects of ginsenoside Rb1 (Rb1) on anthracycline-induced hypertrophy remain unclear. This study aimed to explore the antihypertrophic effect of Rb1 on post-doxorubicin (DOX) treatment myocardial hypertrophy and underlying mechanism.
Methods: Post-DOX treatment myocardial hypertrophy was induced 12 days or 22 h after 15 mg/kg DOX injection in C57BL/6 mice or 2 h DOX (2 μM) incubation in H9c2 cardiomyoblasts. Rb1 was administered 2 days before DOX exposure for 14 consecutive days or 6 h before DOX incubation for 30 h. Heart weight/Body weight (HW/BW), heart weight/tibia length (HW/TL) ratios, echocardiography, WGA staining and the contents of α-SMA, BNP and β-MCH were used to validate myocardial hypertrophy. HE staining, Masson staining, and transmission electron microscopy were performed to assess changes in cardiac morphology. Fluo-3/AM fluorescence was applied to measure the cytosolic free calcium concentration. Western blot, immunohistochemical and immunofluorescence staining were used to assess the expression of CaNBβ/NFATc4/GATA4 signaling.
Results: Rb1 significantly decreased the HW/BW, HW/TL and LVd mass/BW ratios, reduced the cardiomyocyte area and the expression of BNP, β-MHC and α-SMA. Rb1 also relieved myocardial fibrosis and subcellar structure changes and improved the cardiac hemodynamics of post-DOX treatment mice. Rb1 decreased post-DOX treatment calcium overload. Consistent with these findings, in vivo and in vitro CaN, NFATc4 and GATA4 overexpression was rectified.
Conclusion: Rb1 ameliorated post-doxorubicin treatment myocardial hypertrophy, which may be correlated with CaN/NFAT/GATA4 downregulation.
{"title":"Ginsenoside Rb1 ameliorates post-doxorubicin treatment myocardial hypertrophy via CaN/NFATc4/GATA4.","authors":"Jin-Jin Chang, Li-Xia Xu, Wen-Jing Yi, Huan-Huan Zhang, Jun-Wei Zhang, Bin Zheng, Ping-Ying Fu, Rui-Lan He, Rui-Xing Wang, Jian-Feng Jiang, Long-Xin Gui, Min-Xia Wu, Jun-Jin Lin, Zhi-Hong Huang, Jia-Lin Song, Mo-Jun Lin, Hai-Xia Jiao, Zhi-Juan Wu","doi":"10.1016/j.jgr.2025.06.003","DOIUrl":"10.1016/j.jgr.2025.06.003","url":null,"abstract":"<p><strong>Background: </strong>Myocardial hypertrophy is a crucial pathological change that occurs during post-anthracycline treatment cardiomyopathy. The effects of ginsenoside Rb1 (Rb1) on anthracycline-induced hypertrophy remain unclear. This study aimed to explore the antihypertrophic effect of Rb1 on post-doxorubicin (DOX) treatment myocardial hypertrophy and underlying mechanism.</p><p><strong>Methods: </strong>Post-DOX treatment myocardial hypertrophy was induced 12 days or 22 h after 15 mg/kg DOX injection in C57BL/6 mice or 2 h DOX (2 μM) incubation in H9c2 cardiomyoblasts. Rb1 was administered 2 days before DOX exposure for 14 consecutive days or 6 h before DOX incubation for 30 h. Heart weight/Body weight (HW/BW), heart weight/tibia length (HW/TL) ratios, echocardiography, WGA staining and the contents of α-SMA, BNP and β-MCH were used to validate myocardial hypertrophy. HE staining, Masson staining, and transmission electron microscopy were performed to assess changes in cardiac morphology. Fluo-3/AM fluorescence was applied to measure the cytosolic free calcium concentration. Western blot, immunohistochemical and immunofluorescence staining were used to assess the expression of CaNBβ/NFATc4/GATA4 signaling.</p><p><strong>Results: </strong>Rb1 significantly decreased the HW/BW, HW/TL and LVd mass/BW ratios, reduced the cardiomyocyte area and the expression of BNP, β-MHC and α-SMA. Rb1 also relieved myocardial fibrosis and subcellar structure changes and improved the cardiac hemodynamics of post-DOX treatment mice. Rb1 decreased post-DOX treatment calcium overload. Consistent with these findings, <i>in vivo</i> and <i>in vitro</i> CaN, NFATc4 and GATA4 overexpression was rectified.</p><p><strong>Conclusion: </strong>Rb1 ameliorated post-doxorubicin treatment myocardial hypertrophy, which may be correlated with CaN/NFAT/GATA4 downregulation.</p>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 5","pages":"585-593"},"PeriodicalIF":5.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144956985","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}
Pub Date : 2025-09-01Epub Date: 2025-05-02DOI: 10.1016/j.jgr.2025.04.009
Ji Hye Oh, Seung Hwa Baek, Hee Won Seo, Seung Ho Lee, Seock Yeon Hwang
Background: Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer and environmental pollutant that continuously accumulates in the body, causing urogenital toxicity. Further, DEHP accumulation can cause glomerulonephritis due to nephrotoxicity as well as infertility by disturbing reproductive function. Crude saponin is the main active ingredient of ginseng and acts effectively to protect against oxidative stress by activating signaling pathways, such as NF-κB, AP-1 and IRF. Here we investigated the effect of crude-saponin on p38 MAPK/NF-κB signaling against DEHP-induced genitourinary damage in rats.
Methods: We conducted an in vivo reproductive toxicity study in 4-week-old prepubertal SD rats. DEHP was administered orally at 1000 mg/kg/b.w., for 28 days and crude saponin was administered intraperitoneally at 10, 20, and 40 mg/kg/b.w. for 21 days from 1 wk after DEHP exposure. Four weeks later, extensive analysis of the mice's blood and tissues was performed to characterize their response to DEHP and the protective effects of crude saponin.
Results: DEHP induced inflammation, decreased testicular germ cells, and caused damage to renal tubular epithelial cells and infiltration of inflammatory cells. The expression of MCP-1, a chemokine upregulated by MAPK signaling, was significantly increased in the testicular tissue of DEHP-treated rats (68.3 % ± 4.3 %) compared with the NC group (47.3 % ± 9.8 %) (p < 0.05). In contrast, the high-dose crude saponin group showed a decrease of 60.8 % ± 3.3 %, increased testicular germ cells, and alleviated damage to seminiferous tubule epithelial cells. crude saponin alleviated inflammation by regulating MCP-1 and thereby modulating p38 MAPK/NF-κB signaling.
Conclusions: While the precise mechanism underlying the favorable effects of crude saponin remains to be determined, present study provides a basis for the preventive and therapeutic potential of Korean red ginseng against urogenital disorders induced by phthalate-related plasticizer.
{"title":"Crude saponin from Korean red ginseng alleviates di(2-ethylhexyl) phthalate-induced urogenital damage via regulating p38 MAPK/NF-κB signaling.","authors":"Ji Hye Oh, Seung Hwa Baek, Hee Won Seo, Seung Ho Lee, Seock Yeon Hwang","doi":"10.1016/j.jgr.2025.04.009","DOIUrl":"10.1016/j.jgr.2025.04.009","url":null,"abstract":"<p><strong>Background: </strong>Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer and environmental pollutant that continuously accumulates in the body, causing urogenital toxicity. Further, DEHP accumulation can cause glomerulonephritis due to nephrotoxicity as well as infertility by disturbing reproductive function. Crude saponin is the main active ingredient of ginseng and acts effectively to protect against oxidative stress by activating signaling pathways, such as NF-κB, AP-1 and IRF. Here we investigated the effect of crude-saponin on p38 MAPK/NF-κB signaling against DEHP-induced genitourinary damage in rats.</p><p><strong>Methods: </strong>We conducted an <i>in vivo</i> reproductive toxicity study in 4-week-old prepubertal SD rats. DEHP was administered orally at 1000 mg/kg/b.w., for 28 days and crude saponin was administered intraperitoneally at 10, 20, and 40 mg/kg/b.w. for 21 days from 1 wk after DEHP exposure. Four weeks later, extensive analysis of the mice's blood and tissues was performed to characterize their response to DEHP and the protective effects of crude saponin.</p><p><strong>Results: </strong>DEHP induced inflammation, decreased testicular germ cells, and caused damage to renal tubular epithelial cells and infiltration of inflammatory cells. The expression of MCP-1, a chemokine upregulated by MAPK signaling, was significantly increased in the testicular tissue of DEHP-treated rats (68.3 % ± 4.3 %) compared with the NC group (47.3 % ± 9.8 %) (<i>p</i> < 0.05). In contrast, the high-dose crude saponin group showed a decrease of 60.8 % ± 3.3 %, increased testicular germ cells, and alleviated damage to seminiferous tubule epithelial cells. crude saponin alleviated inflammation by regulating MCP-1 and thereby modulating p38 MAPK/NF-κB signaling.</p><p><strong>Conclusions: </strong>While the precise mechanism underlying the favorable effects of crude saponin remains to be determined, present study provides a basis for the preventive and therapeutic potential of Korean red ginseng against urogenital disorders induced by phthalate-related plasticizer.</p>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 5","pages":"532-540"},"PeriodicalIF":5.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957014","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}
Pub Date : 2025-09-01Epub Date: 2025-05-14DOI: 10.1016/j.jgr.2025.05.003
Yuhao Wang, Canglang Mou, Yeye Hu, Ziliang He, Jae Youl Cho, Ji Hye Kim
Ginseng, a traditional herb with a history spanning thousands of years in Asian culture, has gained widespread recognition for its valuable pharmacological properties. The primary active constituents of ginseng, ginsenosides, are renowned for their diverse biological activities, including cardioprotective, anti-tumor, anti-inflammatory, and neuroprotective effects. However, the therapeutic potential of ginsenosides is often constrained by their low bioavailability in their native forms. During metabolism, ginsenosides undergo biotransformation by intestinal microbiota and enzymes, yielding metabolites with significantly enhanced bioavailability. Thus, to enhance the utility of ginsenosides as pharmaceutical agents and health products, it is essential to deepen our understanding of their metabolic processes and bioavailability in vivo. This review provides a comprehensive analysis of the ginsenoside content in ginseng and the modifications that occur during in vivo metabolism. Particular emphasis is placed on the plasma concentrations of ginsenoside metabolites, as well as the pivotal roles of specific microorganisms and enzymes in the metabolic process. Additionally, the pharmacokinetics of ginsenosides in the bloodstream following metabolism and their associated pharmacological activities are thoroughly examined. By offering a detailed exploration of ginsenosides' metabolism and pharmacodynamics, this review aims to advance our understanding of their therapeutic potential and support future research and drug development initiatives.
{"title":"<i>In vivo</i> metabolism, pharmacokinetics, and pharmacological activities of ginsenosides from ginseng.","authors":"Yuhao Wang, Canglang Mou, Yeye Hu, Ziliang He, Jae Youl Cho, Ji Hye Kim","doi":"10.1016/j.jgr.2025.05.003","DOIUrl":"10.1016/j.jgr.2025.05.003","url":null,"abstract":"<p><p>Ginseng, a traditional herb with a history spanning thousands of years in Asian culture, has gained widespread recognition for its valuable pharmacological properties. The primary active constituents of ginseng, ginsenosides, are renowned for their diverse biological activities, including cardioprotective, anti-tumor, anti-inflammatory, and neuroprotective effects. However, the therapeutic potential of ginsenosides is often constrained by their low bioavailability in their native forms. During metabolism, ginsenosides undergo biotransformation by intestinal microbiota and enzymes, yielding metabolites with significantly enhanced bioavailability. Thus, to enhance the utility of ginsenosides as pharmaceutical agents and health products, it is essential to deepen our understanding of their metabolic processes and bioavailability <i>in vivo</i>. This review provides a comprehensive analysis of the ginsenoside content in ginseng and the modifications that occur during <i>in vivo</i> metabolism. Particular emphasis is placed on the plasma concentrations of ginsenoside metabolites, as well as the pivotal roles of specific microorganisms and enzymes in the metabolic process. Additionally, the pharmacokinetics of ginsenosides in the bloodstream following metabolism and their associated pharmacological activities are thoroughly examined. By offering a detailed exploration of ginsenosides' metabolism and pharmacodynamics, this review aims to advance our understanding of their therapeutic potential and support future research and drug development initiatives.</p>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 5","pages":"479-487"},"PeriodicalIF":5.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144956995","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}
Background: Ginsenoside Rb1 is a prominent bioactive component in traditional Chinese medicine.
Purpose: This study investigated the molecular mechanisms underlying the protective effects of Ginsenoside Rb1 on endothelium during ischemia-reperfusion (I/R) injury.
Materials and methods: To enrich for marker genes and investigate the differential expression of DUSP1 and NDUFS4 in coronary artery disease, single-cell transcriptome sequencing was utilized. SIRT5CKO/TG and NDUFS4CKO/TG mouse models were established using gene modification techniques. Si-DUSP-1/ad-DUSP-1 and si-SIRT5/ad-SIRT5 cell models were constructed. Fluorescence detection, mitochondrial membrane potential assays, RT-PCR, and Western blotting were employed to detect the mitochondrial function.
Results: NDUFS4 and DUSP1 regulate the mitochondrial unfolded protein response (mtUPR), energy metabolism, and dynamics, and may be crucial regulatory genes in the development of coronary artery disease. Ginsenoside Rb1 modulates the NDUFS4-SIRT5-DUSP1 axis, regulates the mitochondrial quality control network, and alleviates coronary microvascular inflammatory injury.
Conclusions: Ginsenoside Rb1 regulates the NDUFS4-SIRT5-DUSP1 axis, modulating the mitochondrial quality control network, inhibiting the inflammatory cascade response, and improved myocardial function.
{"title":"Ginsenoside Rb1 attenuates coronary microvascular inflammatory injury via NDUFS4-SIRT5-DUSP1-mediated mitochondrial quality control in a murine ischemia-reperfusion model.","authors":"Xiangyi Pu, Jinfeng Liu, Yanli Wang, Xuanke Guan, Qiaomin Wu, Qin Zhang, Ruxiu Liu, Xing Chang","doi":"10.1016/j.jgr.2025.04.006","DOIUrl":"10.1016/j.jgr.2025.04.006","url":null,"abstract":"<p><strong>Background: </strong>Ginsenoside Rb1 is a prominent bioactive component in traditional Chinese medicine.</p><p><strong>Purpose: </strong>This study investigated the molecular mechanisms underlying the protective effects of Ginsenoside Rb1 on endothelium during ischemia-reperfusion (I/R) injury.</p><p><strong>Materials and methods: </strong>To enrich for marker genes and investigate the differential expression of DUSP1 and NDUFS4 in coronary artery disease, single-cell transcriptome sequencing was utilized. SIRT5<sup>CKO/TG</sup> and NDUFS4<sup>CKO/TG</sup> mouse models were established using gene modification techniques. Si-DUSP-1/ad-DUSP-1 and si-SIRT5/ad-SIRT5 cell models were constructed. Fluorescence detection, mitochondrial membrane potential assays, RT-PCR, and Western blotting were employed to detect the mitochondrial function.</p><p><strong>Results: </strong>NDUFS4 and DUSP1 regulate the mitochondrial unfolded protein response (mtUPR), energy metabolism, and dynamics, and may be crucial regulatory genes in the development of coronary artery disease. Ginsenoside Rb1 modulates the NDUFS4-SIRT5-DUSP1 axis, regulates the mitochondrial quality control network, and alleviates coronary microvascular inflammatory injury.</p><p><strong>Conclusions: </strong>Ginsenoside Rb1 regulates the NDUFS4-SIRT5-DUSP1 axis, modulating the mitochondrial quality control network, inhibiting the inflammatory cascade response, and improved myocardial function.</p>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 5","pages":"509-522"},"PeriodicalIF":5.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957009","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}
Pub Date : 2025-05-16DOI: 10.1016/j.jgr.2025.05.005
Hamid Iqbal , Dong-Kwon Rhee
A hallmark of aging is the progressive decline in resilience to stress and mitochondrial activity. As mitochondrial function decreases with aging, mitochondrial DNA (mtDNA) is shed under apoptotic stress, resulting in a persistent low-level of sterile inflammation (called inflammaging) that induces the aging program. In response to inflammaging, the body activates a compensatory anti-inflammatory response, including the activation of regulatory T (Treg) cells, to prevent excessive tissue damage. Recent studies have highlighted the dysfunction of Treg cells in elderly patients, suggesting that their critical role in the mitigation of aging. Additionally, mitochondrial electron transport chain (ETC) complexes, particularly complexes II and III, are essential for the function of Th1 and Treg cells, respectively. Since centenarians experience less inflammaging, this review aims to explore the anti-aging properties of ginseng. Research has shown that ginseng and its active compounds, ginsenosides, increase Treg cells population in aged mice and convert pro-inflammatory M1 macrophages into anti-inflammatory M2 macrophages. Furthermore, ginseng enhances antioxidant protein expression, decreases reactive oxygen species (ROS) production, restores mitochondrial ATP and membrane potential, and exerts anti-aging effects. Ginseng has been shown to extend lifespan, promote beneficial gut bacteria, and slow cognitive decline through its influence on immune cell circulation. Future research, including clinical trials, is needed to clarify the regulatory effects of ginseng on Treg cells, mitochondrial complexes, and their associated metabolites, as well as the interconnected mechanisms between them.
{"title":"The role of ginseng in aging: Insights into regulatory T cells activation and mitochondrial regulation","authors":"Hamid Iqbal , Dong-Kwon Rhee","doi":"10.1016/j.jgr.2025.05.005","DOIUrl":"10.1016/j.jgr.2025.05.005","url":null,"abstract":"<div><div>A hallmark of aging is the progressive decline in resilience to stress and mitochondrial activity. As mitochondrial function decreases with aging, mitochondrial DNA (mtDNA) is shed under apoptotic stress, resulting in a persistent low-level of sterile inflammation (called inflammaging) that induces the aging program. In response to inflammaging, the body activates a compensatory anti-inflammatory response, including the activation of regulatory T (Treg) cells, to prevent excessive tissue damage. Recent studies have highlighted the dysfunction of Treg cells in elderly patients, suggesting that their critical role in the mitigation of aging. Additionally, mitochondrial electron transport chain (ETC) complexes, particularly complexes II and III, are essential for the function of Th1 and Treg cells, respectively. Since centenarians experience less inflammaging, this review aims to explore the anti-aging properties of ginseng. Research has shown that ginseng and its active compounds, ginsenosides, increase Treg cells population in aged mice and convert pro-inflammatory M1 macrophages into anti-inflammatory M2 macrophages. Furthermore, ginseng enhances antioxidant protein expression, decreases reactive oxygen species (ROS) production, restores mitochondrial ATP and membrane potential, and exerts anti-aging effects. Ginseng has been shown to extend lifespan, promote beneficial gut bacteria, and slow cognitive decline through its influence on immune cell circulation. Future research, including clinical trials, is needed to clarify the regulatory effects of ginseng on Treg cells, mitochondrial complexes, and their associated metabolites, as well as the interconnected mechanisms between them.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 376-388"},"PeriodicalIF":6.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307198","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 : 2025-04-24DOI: 10.1016/j.jgr.2025.04.007
In-Ho Seo , Byoungjin Park , Heejung Kim , Seok-Jae Heo , Dong-Hyuk Jung
Background
In this study, we investigated the therapeutic potential effects of G1899 Korean Red Ginseng Extract Powder(G1899) on long COVID in a general population using flow cytometry and follow-up by questionnaire.
Methods
We conducted a 12-week clinical pilot study on 220 COVID19 patients who were recently infected. The study was completed by 108 participants in the G1899 group and 108 participants in the placebo group. Participants were randomized 1:1 to the G1899 and placebo groups. We evaluated the long COVID by questionnaire including GAD-7, FSS and BFI-K at baseline and 12 weeks. To investigate the changes in the levels of CD4/CD8 T cell ratio and regulatory T cell population, multicolor flow cytometry was performed.
Results
The G1899 group showed significantly chronic fatigue symptoms relieving compared with placebo group at 12 weeks in women. The CD4/CD8 ratio increased significantly in the G1899 group, rising from 1.71 (95 % CI: 1.35–2.07) at Visit 1 to 2.31 (95 % CI: 1.83–2.78) at Visit 4 (p = 0.0029). Unlike the G1899 group, there was a significant reduction in the Treg population, from 2.02 % at Visit 1–1.22 % at Visit 4 (p = 0.0005) in the placebo group.
Conclusion
These findings suggest that G1899 has beneficial effects on the amelioration of long COVID symptoms, with more prominent effects observed in women. Although the changes in Treg population were not statistically significant in the G1899 group, the significant reduction observed in the placebo group suggests a potential protective effect of G1899 against Treg depletion.
{"title":"The effects of G1899 Korean red ginseng extract powder on long COVID for acute COVID19 infection: A randomized, double-blind, placebo-controlled trial","authors":"In-Ho Seo , Byoungjin Park , Heejung Kim , Seok-Jae Heo , Dong-Hyuk Jung","doi":"10.1016/j.jgr.2025.04.007","DOIUrl":"10.1016/j.jgr.2025.04.007","url":null,"abstract":"<div><h3>Background</h3><div>In this study, we investigated the therapeutic potential effects of G1899 Korean Red Ginseng Extract Powder(G1899) on long COVID in a general population using flow cytometry and follow-up by questionnaire.</div></div><div><h3>Methods</h3><div>We conducted a 12-week clinical pilot study on 220 COVID19 patients who were recently infected. The study was completed by 108 participants in the G1899 group and 108 participants in the placebo group. Participants were randomized 1:1 to the G1899 and placebo groups. We evaluated the long COVID by questionnaire including GAD-7, FSS and BFI-K at baseline and 12 weeks. To investigate the changes in the levels of CD4/CD8 T cell ratio and regulatory T cell population, multicolor flow cytometry was performed.</div></div><div><h3>Results</h3><div>The G1899 group showed significantly chronic fatigue symptoms relieving compared with placebo group at 12 weeks in women. The CD4/CD8 ratio increased significantly in the G1899 group, rising from 1.71 (95 % CI: 1.35–2.07) at Visit 1 to 2.31 (95 % CI: 1.83–2.78) at Visit 4 (p = 0.0029). Unlike the G1899 group, there was a significant reduction in the Treg population, from 2.02 % at Visit 1–1.22 % at Visit 4 (p = 0.0005) in the placebo group.</div></div><div><h3>Conclusion</h3><div>These findings suggest that G1899 has beneficial effects on the amelioration of long COVID symptoms, with more prominent effects observed in women. Although the changes in Treg population were not statistically significant in the G1899 group, the significant reduction observed in the placebo group suggests a potential protective effect of G1899 against Treg depletion.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 470-477"},"PeriodicalIF":6.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307029","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 : 2025-04-21DOI: 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":"2025-04-21","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 : 2025-04-15DOI: 10.1016/j.jgr.2025.04.004
Heejun Ha , Heeseon Shin , Sukhyun Min , Natasha Christabella Sutopo , Khamit Yerkesh , Eunsun Jung , Minkyung Song , Jae Youl Cho , Jongsung Lee
The circadian rhythm, a biological system all living organisms possess, has become increasingly important as sleep patterns become more irregular. Circadian rhythms affect various cell types (fibroblasts, fat cells, muscles, etc.) and organs (the liver, pancreas, gut, etc.). This review focuses on the effects of the circadian rhythm on skin physiology. Under normal conditions, the circadian rhythm is involved in maintaining skin health, including DNA repair and wound healing. Disrupted circadian rhythm can cause skin disorders, including hyperpigmentation, melanoma, skin aging, sunburn, impaired wound healing, and an abnormal skin barrier.
Furthermore, the effects of ginsenosides, the primary bioactive component of Panax ginseng, were examined on recovery from skin disorders associated with circadian rhythm disruptions. Therefore, this review explains the relationship between skin physiology and circadian rhythm and suggests the potential of ginseng as a treatment for circadian rhythm-mediated skin disorders.
{"title":"Therapeutic potential of ginsenosides in circadian rhythm-based skin disorders","authors":"Heejun Ha , Heeseon Shin , Sukhyun Min , Natasha Christabella Sutopo , Khamit Yerkesh , Eunsun Jung , Minkyung Song , Jae Youl Cho , Jongsung Lee","doi":"10.1016/j.jgr.2025.04.004","DOIUrl":"10.1016/j.jgr.2025.04.004","url":null,"abstract":"<div><div>The circadian rhythm, a biological system all living organisms possess, has become increasingly important as sleep patterns become more irregular. Circadian rhythms affect various cell types (fibroblasts, fat cells, muscles, etc.) and organs (the liver, pancreas, gut, etc.). This review focuses on the effects of the circadian rhythm on skin physiology. Under normal conditions, the circadian rhythm is involved in maintaining skin health, including DNA repair and wound healing. Disrupted circadian rhythm can cause skin disorders, including hyperpigmentation, melanoma, skin aging, sunburn, impaired wound healing, and an abnormal skin barrier.</div><div>Furthermore, the effects of ginsenosides, the primary bioactive component of <em>Panax ginseng</em>, were examined on recovery from skin disorders associated with circadian rhythm disruptions. Therefore, this review explains the relationship between skin physiology and circadian rhythm and suggests the potential of ginseng as a treatment for circadian rhythm-mediated skin disorders.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 4","pages":"Pages 366-375"},"PeriodicalIF":6.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307034","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 : 2025-04-10DOI: 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":"2025-04-10","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}
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