Pub 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":"2025-03-21","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 : 2025-03-20DOI: 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":"2025-03-20","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 : 2025-02-24DOI: 10.1016/j.jgr.2025.02.002
Yujeong Ha , Hyo-Sung Jo , Tae Woo Kwon , Seung Ho Jeon , Sang-Kwan Moon , Ji Hoon Jung , Min Soo Kim , Seung-Yeol Nah , Jong Kil Lee , Ik-Hyun Cho
Background
Korean black ginseng, a specially processed ginseng through repeat steaming and drying, has various pharmacological effects. However, its role in cognitive impairment remains unclear.
Purpose and methods
This study examined whether Korean black ginseng extract (BGE; 50 and 100 mg/kg, orally, 18 weeks) may mitigate cognitive impairment in a 5xFAD mouse model of Alzheimer's disease (AD).
Results
BGE significantly improved cognitive performance in 5xFAD mice, associated with reduced Aβ accumulation in the frontal cortex and hippocampus. BGE suppressed microglial and astrocytic activation, alongside the downregulation of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and enzymes (cyclooxygenase-2 and inducible nitric oxide synthase). These changes coincided with the inhibition of key inflammatory signaling pathways, such as p38 mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB)/p65, signal transducer and activator of transcription (STAT) 3, and NOD-like receptor protein 3 (NLRP3) inflammasome. Furthermore, BGE reduced the generation of reactive oxygen species and enhanced the nuclear-E2-related factor 2 (Nrf2)-heme oxygenase 1 (HO-1) signaling pathway in the brains linked to the downregulation of toll-like receptors (TLR)-2 and TLR-4 in the brain.
Conclusion
Taken together, BGE could improve AD-related cognitive decline and neurodegeneration by simultaneously regulating anti-inflammatory pathways (p38 MAPK/NF-κB/STAT3 and NLRP3 inflammasome) and an antioxidant pathway (Nrf2/HO-1) via modulation of TLR2/4.
{"title":"Korean black ginseng extract alleviates Alzheimer's disease-related cognitive impairment by activating the Nrf2/HO-1 pathway and suppressing the p38 MAPK/NF-κB/STAT3 pathways and NLRP3 inflammasome via TLR2 and TLR4 modulation","authors":"Yujeong Ha , Hyo-Sung Jo , Tae Woo Kwon , Seung Ho Jeon , Sang-Kwan Moon , Ji Hoon Jung , Min Soo Kim , Seung-Yeol Nah , Jong Kil Lee , Ik-Hyun Cho","doi":"10.1016/j.jgr.2025.02.002","DOIUrl":"10.1016/j.jgr.2025.02.002","url":null,"abstract":"<div><h3>Background</h3><div>Korean black ginseng, a specially processed ginseng through repeat steaming and drying, has various pharmacological effects. However, its role <em>i</em><em>n</em> cognitive impairment remains unclear.</div></div><div><h3>Purpose and methods</h3><div>This study examined whether Korean black ginseng extract (BGE; 50 and 100 mg/kg, orally, 18 weeks) may mitigate cognitive impairment in a 5xFAD mouse model of Alzheimer's disease (AD).</div></div><div><h3>Results</h3><div>BGE significantly improved cognitive performance in 5xFAD mice, associated with reduced Aβ accumulation in the frontal cortex and hippocampus. BGE suppressed microglial and astrocytic activation, alongside the downregulation of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and enzymes (cyclooxygenase-2 and inducible nitric oxide synthase). These changes coincided with the inhibition of key inflammatory signaling pathways, such as p38 mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB)/p65, signal transducer and activator of transcription (STAT) 3, and NOD-like receptor protein 3 (NLRP3) inflammasome. Furthermore, BGE reduced the generation of reactive oxygen species and enhanced the nuclear-E2-related factor 2 (Nrf2)-heme oxygenase 1 (HO-1) signaling pathway in the brains linked to the downregulation of toll-like receptors (TLR)-2 and TLR-4 in the brain.</div></div><div><h3>Conclusion</h3><div>Taken together, BGE could improve AD-related cognitive decline and neurodegeneration by simultaneously regulating anti-inflammatory pathways (p38 MAPK/NF-κB/STAT3 and NLRP3 inflammasome) and an antioxidant pathway (Nrf2/HO-1) via modulation of TLR2/4.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 294-305"},"PeriodicalIF":6.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870184","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 : 2025-02-18DOI: 10.1016/j.jgr.2025.02.003
Lixiao Zhang , Pengfei Chen , Lin Xu , Ming Guo
Coronary artery disease (CAD) is a leading cause of morbidity and mortality globally, necessitating innovative therapeutic strategies. Panax ginseng Meyer, esteemed in traditional Chinese medicine as the “King of Herbs,” has garnered scientific attention for its cardiovascular benefits. Among its bioactive components, ginsenoside Rg1 stands out as a potent therapeutic candidate. This review consolidates current research on Rg1's multifaceted mechanisms in CAD management, including its roles in enhancing endothelial function, inhibiting smooth muscle cell proliferation, modulating inflammation, regulating lipid metabolism, preventing thrombosis, and promoting angiogenesis. Furthermore, Rg1 exhibits cardioprotective properties by mitigating ischemic myocardial injury, reducing myocardial hypertrophy, and preventing fibrosis. Despite promising preclinical findings, the clinical translation of Rg1 is hindered by challenges such as poor bioavailability, potential drug interactions, and limited clinical trial data. This review underscores the need for rigorous clinical studies to validate Rg1's efficacy and safety, paving the way for its incorporation into CAD therapeutic regimens.
{"title":"Roles and mechanisms of ginsenoside Rg1 in coronary artery disease: Progress and perspectives","authors":"Lixiao Zhang , Pengfei Chen , Lin Xu , Ming Guo","doi":"10.1016/j.jgr.2025.02.003","DOIUrl":"10.1016/j.jgr.2025.02.003","url":null,"abstract":"<div><div>Coronary artery disease (CAD) is a leading cause of morbidity and mortality globally, necessitating innovative therapeutic strategies. Panax ginseng Meyer, esteemed in traditional Chinese medicine as the “King of Herbs,” has garnered scientific attention for its cardiovascular benefits. Among its bioactive components, ginsenoside Rg1 stands out as a potent therapeutic candidate. This review consolidates current research on Rg1's multifaceted mechanisms in CAD management, including its roles in enhancing endothelial function, inhibiting smooth muscle cell proliferation, modulating inflammation, regulating lipid metabolism, preventing thrombosis, and promoting angiogenesis. Furthermore, Rg1 exhibits cardioprotective properties by mitigating ischemic myocardial injury, reducing myocardial hypertrophy, and preventing fibrosis. Despite promising preclinical findings, the clinical translation of Rg1 is hindered by challenges such as poor bioavailability, potential drug interactions, and limited clinical trial data. This review underscores the need for rigorous clinical studies to validate Rg1's efficacy and safety, paving the way for its incorporation into CAD therapeutic regimens.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 225-236"},"PeriodicalIF":6.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870505","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 : 2025-02-10DOI: 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":"2025-02-10","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 : 2025-01-30DOI: 10.1016/j.jgr.2025.01.006
Seung-Hwan Seo , Do-Won Ham , Ji-Eun Lee , Seung-Min Jong , Sang-Kyu Kim , Seung-Ho Lee , Hye-Young Yu , Eun-Hee Shin
Background
Obesity is an important risk factor of intestinal inflammatory disease. This study aimed to evaluate the effects of Red ginseng extract powder (RGEP) and Red ginseng dietary fiber (RGDF) on the maintenance of immune and functional homeostasis in recovering obesity-induced impairment of intestinal immunity.
Methods
Diet-induced obesity in C57BL/6 male mice was achieved by feeding them a 60 % high-fat diet for six weeks. The diet-induced obese (DIO) mice were administered RGEP (205, 410, or 820 mg/kg), fructooligosaccharide (FOS, 820 mg/kg), or RGDF (410, 820, or 1640 mg/kg) once daily for 4–8 weeks. The effects of RGEP or RGDF administration were evaluated via stool trait and gastrointestinal (GI) motility, inflammatory biomarkers and cytokines in mesenteric lymph nodes and intestine, mucosal protective genes, bacterial toxicity, and histopathological features of the intestines.
Results
RGEP or RGDF administration to the DIO mice reduced mucosal barrier damaging factor (α1-antitrypsin), inflammatory cytokine levels, factors related to inflammatory responses (C-reactive protein (CRP), iNOS, NF-κB, MPO, and Calprotectin), and levels of urinary indican and intestinal β-glucuronidase. Conversely, RGEP or RGDF administration increased intestinal motility, levels of short-chain fatty acids (SCFAs) and β-defensin-2, and mucus barrier functional factor (MUC2) expression. Histopathological features of the small intestine recovered to normal levels after RGEP or RGDF administration.
Conclusion
Our results demonstrated that RGEP and RGDF were effective for maintaining intestinal immune and functional homeostasis by recovering impaired immune and barrier function in DIO mice.
{"title":"Effects of red ginseng extract and red ginseng dietary fiber on the maintenance of intestinal immune and functional homeostasis in diet-induced obese mice","authors":"Seung-Hwan Seo , Do-Won Ham , Ji-Eun Lee , Seung-Min Jong , Sang-Kyu Kim , Seung-Ho Lee , Hye-Young Yu , Eun-Hee Shin","doi":"10.1016/j.jgr.2025.01.006","DOIUrl":"10.1016/j.jgr.2025.01.006","url":null,"abstract":"<div><h3>Background</h3><div>Obesity is an important risk factor of intestinal inflammatory disease. This study aimed to evaluate the effects of Red ginseng extract powder (RGEP) and Red ginseng dietary fiber (RGDF) on the maintenance of immune and functional homeostasis in recovering obesity-induced impairment of intestinal immunity.</div></div><div><h3>Methods</h3><div>Diet-induced obesity in C57BL/6 male mice was achieved by feeding them a 60 % high-fat diet for six weeks. The diet-induced obese (DIO) mice were administered RGEP (205, 410, or 820 mg/kg), fructooligosaccharide (FOS, 820 mg/kg), or RGDF (410, 820, or 1640 mg/kg) once daily for 4–8 weeks. The effects of RGEP or RGDF administration were evaluated via stool trait and gastrointestinal (GI) motility, inflammatory biomarkers and cytokines in mesenteric lymph nodes and intestine, mucosal protective genes, bacterial toxicity, and histopathological features of the intestines.</div></div><div><h3>Results</h3><div>RGEP or RGDF administration to the DIO mice reduced mucosal barrier damaging factor (α1-antitrypsin), inflammatory cytokine levels, factors related to inflammatory responses (C-reactive protein (CRP), iNOS, NF-κB, MPO, and Calprotectin), and levels of urinary indican and intestinal β-glucuronidase. Conversely, RGEP or RGDF administration increased intestinal motility, levels of short-chain fatty acids (SCFAs) and β-defensin-2, and mucus barrier functional factor (MUC2) expression. Histopathological features of the small intestine recovered to normal levels after RGEP or RGDF administration.</div></div><div><h3>Conclusion</h3><div>Our results demonstrated that RGEP and RGDF were effective for maintaining intestinal immune and functional homeostasis by recovering impaired immune and barrier function in DIO mice.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 271-281"},"PeriodicalIF":6.8,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870182","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 : 2025-01-27DOI: 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":"2025-01-27","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 : 2025-01-24DOI: 10.1016/j.jgr.2025.01.005
Minjeong Kim , Su Hwan Kim , Juewon Kim , Eun-Ju Jin , Shibo Wei , Yunju Jo , Chang-Myung Oh , Ki-Tae Ha , Jong-Hwa Roh , Wan-Gi Kim , Donghyun Cho , Young Jin Choi , Su Myung Jung , Dongryeol Ryu
{"title":"Corrigendum to “Ginsenoside-Re-rich ethanol extract of Panax ginseng berry enhances healthspan extension via mitostasis and NAD metabolism” [J Ginseng Res Volume 49, Issue 1, January 2025, Pages 92–102]","authors":"Minjeong Kim , Su Hwan Kim , Juewon Kim , Eun-Ju Jin , Shibo Wei , Yunju Jo , Chang-Myung Oh , Ki-Tae Ha , Jong-Hwa Roh , Wan-Gi Kim , Donghyun Cho , Young Jin Choi , Su Myung Jung , Dongryeol Ryu","doi":"10.1016/j.jgr.2025.01.005","DOIUrl":"10.1016/j.jgr.2025.01.005","url":null,"abstract":"","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 2","pages":"Page 224"},"PeriodicalIF":6.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445793","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 : 2025-01-19DOI: 10.1016/j.jgr.2025.01.003
Hyosun Jang , Hyewon Kim , Su-Hyun Oh , Yeonghoon Son , Rami Lee , Seung-Yeol Nah , Hae-June Lee
Background
Because the intestine is a radio-sensitive organ in the body, and radiation-induced intestinal injury is a major clinical problem associated with radiotherapy or radiological accidents. Dysfunction of the epithelial barrier leads to bacterial translocation to other organs, resulting in severe inflammation. Recent findings suggest that gintonin (GT) suppresses oxidative stress and inflammation in neuroinflammatory diseases.
Purpose
This study objected to elucidate the mitigating effects of GT on radiation-induced intestinal injury.
Methods
The therapeutic effects of GT were assessed in a mouse model of radiation-induced intestinal injury using histological, immunohistochemical, and real-time PCR. Additionally, the direct effects of GT and NF-E2-related factor 2 (NRF2) activators on radiation-induced epithelial damage were assessed using Caco-2 cell monolayers.
Results
GT treatment reversed radiation-induced body weight loss, attenuated intestinal damage, and inhibited inflammatory response by reducing inflammatory cell infiltration and cytokine expression in the intestines of mice. Additionally, GT treatment activated NRF2 and ameliorated intestinal barrier damage. In vitro experiments showed that GT treatment affected epithelial permeability and intercellular junction expression in Caco-2 cell monolayers under irradiated conditions. Moreover, treatment with NRF2 activator improved epithelial permeability, improved the expression of intercellular junctions in irradiated epithelial cells, and attenuated radiation-induced intestinal injury in a mouse model.
Conclusion
GT maintains epithelial integrity by activating NRF2-mediated antioxidant activity in radiation-induced intestinal epithelial damage of mice. Overall, these results suggest that GT could be a novel therapeutic agent for radiation-induced intestinal damage.
{"title":"Gintonin enhances epithelial barrier function by activating NRF2 pathway in radiation-induced intestinal injury","authors":"Hyosun Jang , Hyewon Kim , Su-Hyun Oh , Yeonghoon Son , Rami Lee , Seung-Yeol Nah , Hae-June Lee","doi":"10.1016/j.jgr.2025.01.003","DOIUrl":"10.1016/j.jgr.2025.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Because the intestine is a radio-sensitive organ in the body, and radiation-induced intestinal injury is a major clinical problem associated with radiotherapy or radiological accidents. Dysfunction of the epithelial barrier leads to bacterial translocation to other organs, resulting in severe inflammation. Recent findings suggest that gintonin (GT) suppresses oxidative stress and inflammation in neuroinflammatory diseases.</div></div><div><h3>Purpose</h3><div>This study objected to elucidate the mitigating effects of GT on radiation-induced intestinal injury.</div></div><div><h3>Methods</h3><div>The therapeutic effects of GT were assessed in a mouse model of radiation-induced intestinal injury using histological, immunohistochemical, and real-time PCR. Additionally, the direct effects of GT and NF-E2-related factor 2 (NRF2) activators on radiation-induced epithelial damage were assessed using Caco-2 cell monolayers.</div></div><div><h3>Results</h3><div>GT treatment reversed radiation-induced body weight loss, attenuated intestinal damage, and inhibited inflammatory response by reducing inflammatory cell infiltration and cytokine expression in the intestines of mice. Additionally, GT treatment activated NRF2 and ameliorated intestinal barrier damage. In vitro experiments showed that GT treatment affected epithelial permeability and intercellular junction expression in Caco-2 cell monolayers under irradiated conditions. Moreover, treatment with NRF2 activator improved epithelial permeability, improved the expression of intercellular junctions in irradiated epithelial cells, and attenuated radiation-induced intestinal injury in a mouse model.</div></div><div><h3>Conclusion</h3><div>GT maintains epithelial integrity by activating NRF2-mediated antioxidant activity in radiation-induced intestinal epithelial damage of mice. Overall, these results suggest that GT could be a novel therapeutic agent for radiation-induced intestinal damage.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 3","pages":"Pages 248-259"},"PeriodicalIF":6.8,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870507","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 : 2025-01-11DOI: 10.1016/j.jgr.2025.01.002
Qi-Rui Hu , Xin-Yi Zhong , Hua Feng , Xu-Chu Li , Zhi-Hong Zhang , Yao Pan , Ting Luo , Ze-Yuan Deng , Fang Chen
Background
The cancer treatments that target tumor associated angiogenesis (TAA) induced by vascular endothelial growth factor A (VEGFA) have become valued. Ginsenoside Rh2 has been proved to inhibit TAA through VEGFA. However, the underlying mechanisms remain unclear. Moreover, the octyl ester derivative of Rh2 (Rh2-O) exhibited better inhibitory effects than Rh2 on liver cancer in our previous researches, which indicated that Rh2-O might also exert inhibitory effects on TAA.
Purpose
To explore the inhibitory effects of Rh2 and Rh2-O on TAA and to investigate the underlying mechanisms.
Method
The inhibitory effects of Rh2 and Rh2-O on TAA were evaluated by conditioned medium, co-culture, and tumor-bearing mice. The network pharmacology was used to explore the possible targets, which were subsequently verified by specific agonists or inhibitors.
Results
Rh2 and Rh2-O could efficiently inhibit TAA in a dose-dependent manner (P < 0.05). Moreover, the enhancement on phosphorylation of PI3K and STAT3 could reverse the inhibitory effects of Rh2 and Rh2-O on TAA while N-acetylcysteine could improve the effects (P < 0.05).
Conclusion
Rh2 and Rh2-O could inhibit TAA via inhibiting the VEGFA, which was mediated by PI3K/STAT3 and PI3K/HIF-1α pathway. Meanwhile the generation of ROS could be a foe for Rh2 and Rh2-O to inhibit TAA.
{"title":"The molecular mechanism of ginsenoside Rh2 and its octyl ester derivative on anti-angiogenesis in cancer treatment: The battle between PI3K and ROS","authors":"Qi-Rui Hu , Xin-Yi Zhong , Hua Feng , Xu-Chu Li , Zhi-Hong Zhang , Yao Pan , Ting Luo , Ze-Yuan Deng , Fang Chen","doi":"10.1016/j.jgr.2025.01.002","DOIUrl":"10.1016/j.jgr.2025.01.002","url":null,"abstract":"<div><h3>Background</h3><div>The cancer treatments that target tumor associated angiogenesis (TAA) induced by vascular endothelial growth factor A (VEGFA) have become valued. Ginsenoside Rh2 has been proved to inhibit TAA through VEGFA. However, the underlying mechanisms remain unclear. Moreover, the octyl ester derivative of Rh2 (Rh2-O) exhibited better inhibitory effects than Rh2 on liver cancer in our previous researches, which indicated that Rh2-O might also exert inhibitory effects on TAA.</div></div><div><h3>Purpose</h3><div>To explore the inhibitory effects of Rh2 and Rh2-O on TAA and to investigate the underlying mechanisms.</div></div><div><h3>Method</h3><div>The inhibitory effects of Rh2 and Rh2-O on TAA were evaluated by conditioned medium, co-culture, and tumor-bearing mice. The network pharmacology was used to explore the possible targets, which were subsequently verified by specific agonists or inhibitors.</div></div><div><h3>Results</h3><div>Rh2 and Rh2-O could efficiently inhibit TAA in a dose-dependent manner (<em>P</em> < 0.05). Moreover, the enhancement on phosphorylation of PI3K and STAT3 could reverse the inhibitory effects of Rh2 and Rh2-O on TAA while N-acetylcysteine could improve the effects (<em>P</em> < 0.05).</div></div><div><h3>Conclusion</h3><div>Rh2 and Rh2-O could inhibit TAA via inhibiting the VEGFA, which was mediated by PI3K/STAT3 and PI3K/HIF-1α pathway. Meanwhile the generation of ROS could be a foe for Rh2 and Rh2-O to inhibit TAA.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 2","pages":"Pages 208-222"},"PeriodicalIF":6.8,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445790","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}
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