Pub Date : 2025-11-01DOI: 10.1016/j.jgr.2025.06.001
Hyeon Jin Kim , Jae Youl Cho , Mi-Yeon Kim
Unresolved inflammation can progress into severe diseases that need safer and more effective therapeutic strategies. The adverse effects of conventional anti-inflammatory agents have evoked interest in natural products as alternatives. Panax ginseng is a traditional medical herb famous for its diverse pharmacological properties. This review comprehensively discusses the anti-inflammatory effects of P. ginseng and its constituents against inflammatory bowel disease, hepatitis, sepsis, gastritis, atopic dermatitis, acute lung disease, and rheumatoid arthritis. We summarize the therapeutic effects and underlying molecular mechanisms of P. ginseng reported in studies published as of February 2025. Our review highlights the potential of P. ginseng as an anti-inflammatory agent or functional food that affects the interconnected disease network.
{"title":"A comprehensive review of the effects of Panax ginseng and its constituents against inflammatory diseases","authors":"Hyeon Jin Kim , Jae Youl Cho , Mi-Yeon Kim","doi":"10.1016/j.jgr.2025.06.001","DOIUrl":"10.1016/j.jgr.2025.06.001","url":null,"abstract":"<div><div>Unresolved inflammation can progress into severe diseases that need safer and more effective therapeutic strategies. The adverse effects of conventional anti-inflammatory agents have evoked interest in natural products as alternatives. <em>Panax ginseng</em> is a traditional medical herb famous for its diverse pharmacological properties. This review comprehensively discusses the anti-inflammatory effects of <em>P. ginseng</em> and its constituents against inflammatory bowel disease, hepatitis, sepsis, gastritis, atopic dermatitis, acute lung disease, and rheumatoid arthritis. We summarize the therapeutic effects and underlying molecular mechanisms of <em>P. ginseng</em> reported in studies published as of February 2025. Our review highlights the potential of <em>P. ginseng</em> as an anti-inflammatory agent or functional food that affects the interconnected disease network.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 605-612"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435513","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.09.003
Pengcheng Liu , Teng Yang , Jie Zhang , Bang Su , Qidong Shi , Yao Song , Xin Yu
Background
Diabetic peripheral neuropathy (DPN) represents a prevalent complication associated with diabetes mellitus, characterized by progressive nerve degeneration that leads to chronic pain and sensory dysfunction. Existing treatment options are inadequate in addressing the multifaceted underlying mechanisms of DPN, underscoring the necessity for the development of novel multitarget therapeutic strategies.
Methods
A systematic evaluation explored Panax ginseng's (GS) therapeutic efficacy using a multidisciplinary approach, administering the extract to diabetic rats for nerve assessments and conducting in vitro tests on Schwann cells and ND7/23 neuron cells under high glucose. Network pharmacology and molecular docking identified key targets and pathways, validated through experiments on mitochondrial function, oxidative stress, inflammation, and apoptosis.
Results
Administration of GS significantly improved motor nerve conduction velocity, increased pain thresholds, and restored myelination in DPN rats. In vitro, GS enhanced RSC96 and ND7/23 cell viability and migration. Network pharmacology indicated GS modulates RAGE/NF-κB and Nrf2/PPARγ pathways, reducing oxidative stress, enhancing mitochondrial function, and lowering inflammatory cytokines. It also normalizes the Bcl2/Bax ratio to mitigate apoptosis.
Conclusion
The findings of this study illustrate that GS mitigates DPN through a synergistic modulation of mitochondrial function, oxidative stress, neuroinflammation, and apoptosis pathways, with particularly significant effects on maintaining Schwann cell and Neuron cell functionality. Our results provide mechanistic insights that advocate for the repurposing of whole GS extract as a multitarget therapeutic agent for managing diabetic complications.
{"title":"Panax ginseng alleviates diabetic peripheral neuropathy by suppressing mitochondrial dysfunction and oxidative stress via modulation of the RAGE, NF-κB, and Nrf2 pathways","authors":"Pengcheng Liu , Teng Yang , Jie Zhang , Bang Su , Qidong Shi , Yao Song , Xin Yu","doi":"10.1016/j.jgr.2025.09.003","DOIUrl":"10.1016/j.jgr.2025.09.003","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic peripheral neuropathy (DPN) represents a prevalent complication associated with diabetes mellitus, characterized by progressive nerve degeneration that leads to chronic pain and sensory dysfunction. Existing treatment options are inadequate in addressing the multifaceted underlying mechanisms of DPN, underscoring the necessity for the development of novel multitarget therapeutic strategies.</div></div><div><h3>Methods</h3><div>A systematic evaluation explored <em>Panax ginseng</em>'s (GS) therapeutic efficacy using a multidisciplinary approach, administering the extract to diabetic rats for nerve assessments and conducting in vitro tests on Schwann cells and ND7/23 neuron cells under high glucose. Network pharmacology and molecular docking identified key targets and pathways, validated through experiments on mitochondrial function, oxidative stress, inflammation, and apoptosis.</div></div><div><h3>Results</h3><div>Administration of GS significantly improved motor nerve conduction velocity, increased pain thresholds, and restored myelination in DPN rats. In vitro, GS enhanced RSC96 and ND7/23 cell viability and migration. Network pharmacology indicated GS modulates RAGE/NF-κB and Nrf2/PPARγ pathways, reducing oxidative stress, enhancing mitochondrial function, and lowering inflammatory cytokines. It also normalizes the Bcl2/Bax ratio to mitigate apoptosis.</div></div><div><h3>Conclusion</h3><div>The findings of this study illustrate that GS mitigates DPN through a synergistic modulation of mitochondrial function, oxidative stress, neuroinflammation, and apoptosis pathways, with particularly significant effects on maintaining Schwann cell and Neuron cell functionality. Our results provide mechanistic insights that advocate for the repurposing of whole GS extract as a multitarget therapeutic agent for managing diabetic complications.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 734-745"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435268","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.09.004
Suyoung Choi , Thi Thuy Duong Pham , Tae-Keun Jeong , Ju-Gyeong Kang , Sang-Woo Lee , Bu Yeon Heo , Jung-Hyun Park , Jeong Suk Koh , Myung-Won Lee , Dae-Sik Lim , Ik-Chan Song , Jaeyul Kwon
Background
Food allergy (FA) is a growing health concern with limited therapeutic options. While Korean Red Ginseng Extract (KRGE) exhibits immunomodulatory and microbiota-modulating properties, its specific effects and mechanisms in FA are not fully understood.
Methods
We evaluated the anti-allergic efficacy of KRGE in IL4raF709 mice, a model genetically predisposed to IgE-mediated anaphylaxis. Mice were sensitized with ovalbumin(OVA) and staphylococcal enterotoxin B (SEB) and challenged with OVA. KRGE was administered orally prior to and during sensitization. Clinical symptoms, serum IgE levels, IL-33 levels, and intestinal histology were assessed. Mesenteric lymph nodes and Peyer's patches immune cell populations were analyzed by flow cytometry. Fecal microbiota composition was profiled using 16S rRNA sequencing and quantitative PCR; correlations between phenotype and microbiota were investigated.
Results
Results showed KRGE significantly suppressed anaphylactic symptoms, including hypothermia and mortality, and reduced OVA-specific IgE and IL-33 levels. KRGE restored intestinal epithelial integrity and normalized Peyer's patch hypertrophy. Immunologically, it decreased IL-13-producing T follicular helper cells and rebalanced dendritic cell subsets, increasing tolerogenic CD103+ cDC1 and reducing pro-allergic CD11b+ cDC2. Microbiome analysis revealed that OVA/SEB increased pro-inflammatory Lachnospiraceae and Ruminococcaceae while depleting beneficial Lactobacillaceae and Bifidobacteriaceae. KRGE reversed these changes, notably enriching Akkermansia muciniphila and Lactobacillus gasseri. Correlation analysis revealed that Akkermansia, Lactobacillus, and Christensenellaceae were negatively correlated with allergic markers and positively correlated with epithelial integrity. In contrast, Oscillospiraceae (Eubacterium_g8, Acetobacter, and Pseudoflavonifractor) was associated with allergy exacerbation.
Conclusion
KRGE mitigates FA in IL4raF709 mice by restoring gut microbiota balance and immune homeostasis, suggesting its potential as a microbiota-targeted intervention for FA.
{"title":"Korean red ginseng extract suppresses food allergy by remodeling the gut microbiota and restoring immune homeostasis in IL4raF709 mice","authors":"Suyoung Choi , Thi Thuy Duong Pham , Tae-Keun Jeong , Ju-Gyeong Kang , Sang-Woo Lee , Bu Yeon Heo , Jung-Hyun Park , Jeong Suk Koh , Myung-Won Lee , Dae-Sik Lim , Ik-Chan Song , Jaeyul Kwon","doi":"10.1016/j.jgr.2025.09.004","DOIUrl":"10.1016/j.jgr.2025.09.004","url":null,"abstract":"<div><h3>Background</h3><div>Food allergy (FA) is a growing health concern with limited therapeutic options. While Korean Red Ginseng Extract (KRGE) exhibits immunomodulatory and microbiota-modulating properties, its specific effects and mechanisms in FA are not fully understood.</div></div><div><h3>Methods</h3><div>We evaluated the anti-allergic efficacy of KRGE in IL4ra<sup>F709</sup> mice, a model genetically predisposed to IgE-mediated anaphylaxis. Mice were sensitized with ovalbumin(OVA) and staphylococcal enterotoxin B (SEB) and challenged with OVA. KRGE was administered orally prior to and during sensitization. Clinical symptoms, serum IgE levels, IL-33 levels, and intestinal histology were assessed. Mesenteric lymph nodes and Peyer's patches immune cell populations were analyzed by flow cytometry. Fecal microbiota composition was profiled using 16S rRNA sequencing and quantitative PCR; correlations between phenotype and microbiota were investigated.</div></div><div><h3>Results</h3><div>Results showed KRGE significantly suppressed anaphylactic symptoms, including hypothermia and mortality, and reduced OVA-specific IgE and IL-33 levels. KRGE restored intestinal epithelial integrity and normalized Peyer's patch hypertrophy. Immunologically, it decreased IL-13-producing T follicular helper cells and rebalanced dendritic cell subsets, increasing tolerogenic CD103<sup>+</sup> cDC1 and reducing pro-allergic CD11b<sup>+</sup> cDC2. Microbiome analysis revealed that OVA/SEB increased pro-inflammatory <em>Lachnospiraceae</em> and <em>Ruminococcaceae</em> while depleting beneficial <em>Lactobacillaceae</em> and <em>Bifidobacteriaceae</em>. KRGE reversed these changes, notably enriching <em>Akkermansia muciniphila</em> and <em>Lactobacillus gasseri</em>. Correlation analysis revealed that Akkermansia, Lactobacillus, and Christensenellaceae were negatively correlated with allergic markers and positively correlated with epithelial integrity. In contrast, Oscillospiraceae (Eubacterium_g8, Acetobacter, and Pseudoflavonifractor) was associated with allergy exacerbation.</div></div><div><h3>Conclusion</h3><div>KRGE mitigates FA in IL4ra<sup>F709</sup> mice by restoring gut microbiota balance and immune homeostasis, suggesting its potential as a microbiota-targeted intervention for FA.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 746-757"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435312","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.10.004
Ya-Ni Wang , De-Yu Wang , Yu-Hui Li , Cheng-Yan He , Xu-Ming Li , Yang Li , Ying-Hua Jin
Background
Chronic and excessive alcohol consumption is a primary driver of alcohol-associated liver disease (ALD), a global health challenge with limited treatment options. Panax ginseng Meyer exhibits various pharmacological activities, including antioxidant and anti-inflammatory effects. However, its efficacy in preventing alcohol-induced liver injury remains limited, necessitating further optimization and investigation.
Methods
This study evaluated the hepatoprotective effects of Li-Ginseng Powder (LGP), a ginseng preparation enriched in rare ginsenosides, using a murine model of ALD and ethanol-exposed human hepatic L-02 cells. ALD was induced in C57BL/6 mice via daily oral ethanol administration (2400 mg/kg). Serum and liver biochemical markers were measured, and histological changes were assessed using H&E and Oil Red O staining. In vitro assays examined the effects of LGP on ethanol-metabolizing enzyme activity, oxidative stress, mitochondrial integrity, and autophagy.
Results
Ethanol exposure significantly elevated serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, low-density lipoprotein, and cholesterol, as well as hepatic triglycerides and malondialdehyde, while markedly decreasing hepatic levels of reduced glutathione and superoxide dismutase. LGP pre-treatment effectively reversed all these alterations, restored antioxidant capacity, and alleviated histological damage and lipid accumulation to near normal levels. In L-02 cells, LGP significantly enhanced alcohol dehydrogenase and aldehyde dehydrogenase activities, facilitated ethanol and acetaldehyde detoxification, reduced reactive oxygen species levels, preserved mitochondrial membrane potential, and promoted autophagy.
Conclusion
LGP confers comprehensive hepatoprotection against alcohol-induced liver injury by significantly enhancing ethanol catabolism, enhancing antioxidant defenses, and activating autophagy. These findings suggest its therapeutic potential in the management of ALD.
{"title":"Li-Ginseng powder protects against alcohol-induced liver injury by promoting acetaldehyde clearance and cellular homeostasis","authors":"Ya-Ni Wang , De-Yu Wang , Yu-Hui Li , Cheng-Yan He , Xu-Ming Li , Yang Li , Ying-Hua Jin","doi":"10.1016/j.jgr.2025.10.004","DOIUrl":"10.1016/j.jgr.2025.10.004","url":null,"abstract":"<div><h3>Background</h3><div>Chronic and excessive alcohol consumption is a primary driver of alcohol-associated liver disease (ALD), a global health challenge with limited treatment options. Panax ginseng Meyer exhibits various pharmacological activities, including antioxidant and anti-inflammatory effects. However, its efficacy in preventing alcohol-induced liver injury remains limited, necessitating further optimization and investigation.</div></div><div><h3>Methods</h3><div>This study evaluated the hepatoprotective effects of Li-Ginseng Powder (LGP), a ginseng preparation enriched in rare ginsenosides, using a murine model of ALD and ethanol-exposed human hepatic L-02 cells. ALD was induced in C57BL/6 mice via daily oral ethanol administration (2400 mg/kg). Serum and liver biochemical markers were measured, and histological changes were assessed using H&E and Oil Red O staining. In vitro assays examined the effects of LGP on ethanol-metabolizing enzyme activity, oxidative stress, mitochondrial integrity, and autophagy.</div></div><div><h3>Results</h3><div>Ethanol exposure significantly elevated serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, low-density lipoprotein, and cholesterol, as well as hepatic triglycerides and malondialdehyde, while markedly decreasing hepatic levels of reduced glutathione and superoxide dismutase. LGP pre-treatment effectively reversed all these alterations, restored antioxidant capacity, and alleviated histological damage and lipid accumulation to near normal levels. In L-02 cells, LGP significantly enhanced alcohol dehydrogenase and aldehyde dehydrogenase activities, facilitated ethanol and acetaldehyde detoxification, reduced reactive oxygen species levels, preserved mitochondrial membrane potential, and promoted autophagy.</div></div><div><h3>Conclusion</h3><div>LGP confers comprehensive hepatoprotection against alcohol-induced liver injury by significantly enhancing ethanol catabolism, enhancing antioxidant defenses, and activating autophagy. These findings suggest its therapeutic potential in the management of ALD.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 758-766"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435313","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.07.001
Kang Zhou, Huanghe Yu, Huihong Duan, Yupei Yang, Wenbing Sheng, Yixing Qiu, Wei Wang, Bin Li
Background
Heightened glycolysis-driven activation of pro-inflammatory M1 macrophages is a characteristic of rheumatoid arthritis (RA). Dysbiosis of the intestinal microbiota is considered a trigger for the immune response in RA. Panax japonicus is used in ethnomedicine to treat RA, but its molecular mechanisms regarding macrophage polarization and the intestinal microbiota remain to be explored.
Methods
In vitro and in vivo models were established using lipopolysaccharide (LPS)-induced RAW 264.7 macrophage cells and adjuvant-induced arthritis (AIA) rats, and treated with total saponins from Panax japonicus (TSPJ). Inflammatory cytokines were quantified by enzyme-linked immunosorbent assay (ELISA). Glucose, lactate, and LPS were measured by biochemical kits. The M1/M2a ratio in RAW 264.7 cells was assessed by flow cytometry. Joint bone erosion was evaluated by micro-CT. Immunohistochemistry and western blotting were used to evaluate glycolytic regulators in rat joints. Colonic contents and mucosa were analyzed by 16S rRNA sequencing.
Results
TSPJ inhibited inflammatory response, lactate production, and glucose consumption in M1 macrophages, and restored the M2a/M1 balance. In vivo, TSPJ alleviated joint swelling in AIA rats, reduced serum inflammatory cytokines, lactate, and LPS levels, while increasing anti-inflammatory cytokine levels. The protein expressions of hypoxia-inducible factor-1α (HIF-1α), glucose transporter 1 (GLUT1), hexokina se 2 (HK2), and lactate dehydrogenase A (LDHA) in the ankle joints were down-regulated after TSPJ intervention. Furthermore, TSPJ restored microbiota diversity and community structure, and enriched probiotic abundances like Eubacterium_coprostanoligenes_group and Christensenella.
Conclusion
TSPJ alleviates arthritis by inhibiting glycolysis pathway in M1 macrophages, modulating colon microbiota, and promoting the abundance of mucosa-associated probiotics.
{"title":"Total saponins of Panax japonicus alleviate adjuvant-induced arthritis in rats by regulating macrophage polarization and intestinal microbiota","authors":"Kang Zhou, Huanghe Yu, Huihong Duan, Yupei Yang, Wenbing Sheng, Yixing Qiu, Wei Wang, Bin Li","doi":"10.1016/j.jgr.2025.07.001","DOIUrl":"10.1016/j.jgr.2025.07.001","url":null,"abstract":"<div><h3>Background</h3><div>Heightened glycolysis-driven activation of pro-inflammatory M1 macrophages is a characteristic of rheumatoid arthritis (RA). Dysbiosis of the intestinal microbiota is considered a trigger for the immune response in RA. <em>Panax japonicus</em> is used in ethnomedicine to treat RA, but its molecular mechanisms regarding macrophage polarization and the intestinal microbiota remain to be explored.</div></div><div><h3>Methods</h3><div>In <em>vitro</em> and in <em>vivo</em> models were established using lipopolysaccharide (LPS)-induced RAW 264.7 macrophage cells and adjuvant-induced arthritis (AIA) rats, and treated with total saponins from <em>Panax japonicus</em> (TSPJ). Inflammatory cytokines were quantified by enzyme-linked immunosorbent assay (ELISA). Glucose, lactate, and LPS were measured by biochemical kits. The M1/M2a ratio in RAW 264.7 cells was assessed by flow cytometry. Joint bone erosion was evaluated by micro-CT. Immunohistochemistry and western blotting were used to evaluate glycolytic regulators in rat joints. Colonic contents and mucosa were analyzed by 16S rRNA sequencing.</div></div><div><h3>Results</h3><div>TSPJ inhibited inflammatory response, lactate production, and glucose consumption in M1 macrophages, and restored the M2a/M1 balance. In <em>vivo</em>, TSPJ alleviated joint swelling in AIA rats, reduced serum inflammatory cytokines, lactate, and LPS levels, while increasing anti-inflammatory cytokine levels. The protein expressions of hypoxia-inducible factor-1α (HIF-1α), glucose transporter 1 (GLUT1), hexokina se 2 (HK2), and lactate dehydrogenase A (LDHA) in the ankle joints were down-regulated after TSPJ intervention. Furthermore, TSPJ restored microbiota diversity and community structure, and enriched probiotic abundances like <em>Eubacterium_coprostanoligenes_group</em> and <em>Christensenella</em>.</div></div><div><h3>Conclusion</h3><div>TSPJ alleviates arthritis by inhibiting glycolysis pathway in M1 macrophages, modulating colon microbiota, and promoting the abundance of mucosa-associated probiotics.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 692-701"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435254","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.08.003
Weimin Wang , Kaixuan Zhou , Zengshuai Fu , Yucheng Huang , Jianjun Deng , Daidi Fan , Haixia Yang
Background
Alcohol-induced liver injury contributes to various liver diseases, with dietary interventions of ginsenosides being a promising solution. Ginsenosides, the major active compounds of Panax ginseng Meyer, are divided into protopanaxadiol (PPD) and protopanaxatriol (PPT) based on C-3 or C-6 glycosylation, which have anti-inflammatory and antioxidant effects, but structure-activity relationships remain unclear.
Methods
Using C57BL/C mice with alcohol-induced liver injury, we evaluated Rg5 and F4 effects on liver function, inflammation, lipid deposition, apoptosis, alcohol metabolism, and lipid synthesis.
Results
Rg5 (60 mg/kg) demonstrated significantly superior efficacy to F4 in alleviating alcohol-induced liver injury, reducing lipid deposition through 33.9 % and 25.8 % decreases in serum triglyceride (TG) and total cholesterol (TC) levels versus the F4 group. Additionally, Rg5 attenuated hepatic apoptosis by reducing BAX and cleaved-CASPASE-3 protein expression by 26.3 % and 28.4 % compared to F4. Rg5 enhanced alcohol metabolism through activation of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH), thereby restoring AMP-activated protein kinase (AMPK) phosphorylation by 26.1 % while reducing sterol regulatory element-binding protein 1 (SREBP-1) expression by 27.8 % (compared to F4), with efficacy approaching that of positive control silymarin. Molecular docking revealed that the C-6 sugar moiety of F4 induced hydrogen bond donor repulsion, increasing hydrogen bond length and weakening binding stability with ADH, ALDH and AMPK, providing a structural basis for Rg5's superior hepatoprotective activity.
Conclusion
These findings highlight the critical influence of glycosylation position on hepatoprotective activity of ginsenosides, and provide insights into the structural modification of ginsenosides, which could contribute to the treatment of alcohol-related liver disease.
{"title":"Comparison of different ginsenosides with C-3 or C-6 sugar moieties on activities in alcohol-induced liver injury mice","authors":"Weimin Wang , Kaixuan Zhou , Zengshuai Fu , Yucheng Huang , Jianjun Deng , Daidi Fan , Haixia Yang","doi":"10.1016/j.jgr.2025.08.003","DOIUrl":"10.1016/j.jgr.2025.08.003","url":null,"abstract":"<div><h3>Background</h3><div>Alcohol-induced liver injury contributes to various liver diseases, with dietary interventions of ginsenosides being a promising solution. Ginsenosides, the major active compounds of <em>Panax ginseng Meyer</em>, are divided into protopanaxadiol (PPD) and protopanaxatriol (PPT) based on C-3 or C-6 glycosylation, which have anti-inflammatory and antioxidant effects, but structure-activity relationships remain unclear.</div></div><div><h3>Methods</h3><div>Using C57BL/C mice with alcohol-induced liver injury, we evaluated Rg5 and F4 effects on liver function, inflammation, lipid deposition, apoptosis, alcohol metabolism, and lipid synthesis.</div></div><div><h3>Results</h3><div>Rg5 (60 mg/kg) demonstrated significantly superior efficacy to F4 in alleviating alcohol-induced liver injury, reducing lipid deposition through 33.9 % and 25.8 % decreases in serum triglyceride (TG) and total cholesterol (TC) levels versus the F4 group. Additionally, Rg5 attenuated hepatic apoptosis by reducing BAX and cleaved-CASPASE-3 protein expression by 26.3 % and 28.4 % compared to F4. Rg5 enhanced alcohol metabolism through activation of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH), thereby restoring AMP-activated protein kinase (AMPK) phosphorylation by 26.1 % while reducing sterol regulatory element-binding protein 1 (SREBP-1) expression by 27.8 % (compared to F4), with efficacy approaching that of positive control silymarin. Molecular docking revealed that the C-6 sugar moiety of F4 induced hydrogen bond donor repulsion, increasing hydrogen bond length and weakening binding stability with ADH, ALDH and AMPK, providing a structural basis for Rg5's superior hepatoprotective activity.</div></div><div><h3>Conclusion</h3><div>These findings highlight the critical influence of glycosylation position on hepatoprotective activity of ginsenosides, and provide insights into the structural modification of ginsenosides, which could contribute to the treatment of alcohol-related liver disease.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 714-724"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435266","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.08.010
BaiCheng Chen, Ajay Vijayakumar, Jun Hong Park, Chang Won Kang, Jong-Hoon Kim
Korean red ginseng (KRG) and Cervi Parvum Cornu (CPC) act synergistically to improve cyclophosphamide-induced immunosuppression in rats, as evidenced by restoration of lymphocyte numbers, enhanced NK cell cytotoxic activity, normalization of NK cell-related cytokine profiles, and activation of the MAPK signaling pathway.
{"title":"Immunomodulatory effects of the combination of Korean red ginseng and Cervi Parvum Cornu via the MAPK pathway","authors":"BaiCheng Chen, Ajay Vijayakumar, Jun Hong Park, Chang Won Kang, Jong-Hoon Kim","doi":"10.1016/j.jgr.2025.08.010","DOIUrl":"10.1016/j.jgr.2025.08.010","url":null,"abstract":"<div><div>Korean red ginseng (KRG) and Cervi Parvum Cornu (CPC) act synergistically to improve cyclophosphamide-induced immunosuppression in rats, as evidenced by restoration of lymphocyte numbers, enhanced NK cell cytotoxic activity, normalization of NK cell-related cytokine profiles, and activation of the MAPK signaling pathway.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 776-780"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435315","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.08.007
Zhiyong Zhai, Yan Gao
Cerebral small vessel disease (CSVD), an age-related vascular disorder linked to cognitive decline, lacks targeted therapies. Ginsenosides, bioactive compounds in ginseng, demonstrate multi-target potential against CSVD by modulating neurovascular dysfunction. Experimental studies highlight their anti-inflammatory, antioxidant, and neuroprotective properties. Ginsenosides suppress pro-inflammatory cytokines (tumor necrosis factor α [TNF-α], interleukin-1β [IL-1β], IL-6) via nuclear factor-kappa B/nod-like receptor protein (NF-κB/NLRP1) inflammasome inhibition, stabilize the blood-brain barrier by preserving tight junctions and reducing matrix metalloproteinase activity, and enhance endothelial survival through vascular endothelial growth factor/sonic hedgehog (VEGF/Shh)-mediated angiogenesis. They mitigate vascular remodeling by blocking vascular smooth muscle cell (VSMC) proliferation via phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase (MAPK) signaling, while attenuating microglial activation and astrocyte dysfunction to improve cerebral blood flow. These compounds also alleviate oxidative stress and promote neurovascular unit integrity. Future research should focus on optimizing ginsenoside combinations, elucidating protein interactions, and exploring synergies with complementary agents to enhance therapeutic efficacy. Ginsenosides represent a promising multi-mechanistic approach for CSVD treatment, addressing inflammation, vascular pathology, and neural damage.
{"title":"Protective effects of ginsenosides in cerebral small vessel disease: Cellular and molecular mechanisms","authors":"Zhiyong Zhai, Yan Gao","doi":"10.1016/j.jgr.2025.08.007","DOIUrl":"10.1016/j.jgr.2025.08.007","url":null,"abstract":"<div><div>Cerebral small vessel disease (CSVD), an age-related vascular disorder linked to cognitive decline, lacks targeted therapies. Ginsenosides, bioactive compounds in ginseng, demonstrate multi-target potential against CSVD by modulating neurovascular dysfunction. Experimental studies highlight their anti-inflammatory, antioxidant, and neuroprotective properties. Ginsenosides suppress pro-inflammatory cytokines (tumor necrosis factor α [TNF-α], interleukin-1β [IL-1β], IL-6) via nuclear factor-kappa B/nod-like receptor protein (NF-κB/NLRP1) inflammasome inhibition, stabilize the blood-brain barrier by preserving tight junctions and reducing matrix metalloproteinase activity, and enhance endothelial survival through vascular endothelial growth factor/sonic hedgehog (VEGF/Shh)-mediated angiogenesis. They mitigate vascular remodeling by blocking vascular smooth muscle cell (VSMC) proliferation via phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase (MAPK) signaling, while attenuating microglial activation and astrocyte dysfunction to improve cerebral blood flow. These compounds also alleviate oxidative stress and promote neurovascular unit integrity. Future research should focus on optimizing ginsenoside combinations, elucidating protein interactions, and exploring synergies with complementary agents to enhance therapeutic efficacy. Ginsenosides represent a promising multi-mechanistic approach for CSVD treatment, addressing inflammation, vascular pathology, and neural damage.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 640-651"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435517","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.05.009
Ga Rin Gu , Hyeon Jin Kim , Won Young Jang , Hyun Kyung Lim , Ji Yeon Hwang , Yena Oh , Jieun Oh , Soo-Hyun Youn , Sun Hee Hyun , Ji Hye Park , Hun-kun Ko , Seung Ho Lee , Jaehyeon Hwang , Seokoh Moon , Dae-Hyuk Kweon , Jae Youl Cho , Han Gyung Kim
Objective
and design: This research was conducted to investigate the immunomodulatory and anti-inflammatory effects of Korean red ginseng in a low-dose pseudo-type SARS-CoV-2 (PSV) infection model using hACE2 transgenic mice.
Material or subjects
K18-hACE2 transgenic mice were used as an experimental model, and three different Korean red ginseng formulations (non-saponin, saponin, and whole Korean red ginseng extract) were administered prior to infection with the virus.
Methods
The physiological and immunological effects of the Korean red ginseng formulations were assessed by monitoring lung histopathology and luciferase activity in lung tissue. Flow cytometry was used to analyze the populations of immune cells in both the lungs and spleen, and serum IgM levels were quantified using an enzyme-linked immunosorbent assay.
Results
Low-dose PSV infection induced lung injury and immune cell infiltration in the lung. Administration of Korean red ginseng, particularly the saponin fraction, significantly reduced the excessive activation of interstitial macrophages, NK cells, and cytotoxic T cells. Additionally, Korean red ginseng promoted long-term immune memory by increasing the population of memory B cells and cytotoxic T cells in the spleen. In the treatment groups, IgM production was enhanced upon secondary PSV infection.
Conclusions
Korean red ginseng modulates immune responses and promotes long-term immunity against low-dose PSV infection. Our data also support the potential of Korean red ginseng as a complementary therapeutic strategy for COVID-19 and an enhancer of vaccine efficacy.
{"title":"Korean red ginseng mitigates pulmonary injury and enhances antiviral immunity in a low-dose pseudo-type SARS-CoV-2 infection model","authors":"Ga Rin Gu , Hyeon Jin Kim , Won Young Jang , Hyun Kyung Lim , Ji Yeon Hwang , Yena Oh , Jieun Oh , Soo-Hyun Youn , Sun Hee Hyun , Ji Hye Park , Hun-kun Ko , Seung Ho Lee , Jaehyeon Hwang , Seokoh Moon , Dae-Hyuk Kweon , Jae Youl Cho , Han Gyung Kim","doi":"10.1016/j.jgr.2025.05.009","DOIUrl":"10.1016/j.jgr.2025.05.009","url":null,"abstract":"<div><h3>Objective</h3><div><em>and design</em>: This research was conducted to investigate the immunomodulatory and anti-inflammatory effects of Korean red ginseng in a low-dose pseudo-type SARS-CoV-2 (PSV) infection model using hACE2 transgenic mice.</div></div><div><h3>Material or subjects</h3><div>K18-hACE2 transgenic mice were used as an experimental model, and three different Korean red ginseng formulations (non-saponin, saponin, and whole Korean red ginseng extract) were administered prior to infection with the virus.</div></div><div><h3>Methods</h3><div>The physiological and immunological effects of the Korean red ginseng formulations were assessed by monitoring lung histopathology and luciferase activity in lung tissue. Flow cytometry was used to analyze the populations of immune cells in both the lungs and spleen, and serum IgM levels were quantified using an enzyme-linked immunosorbent assay.</div></div><div><h3>Results</h3><div>Low-dose PSV infection induced lung injury and immune cell infiltration in the lung. Administration of Korean red ginseng, particularly the saponin fraction, significantly reduced the excessive activation of interstitial macrophages, NK cells, and cytotoxic T cells. Additionally, Korean red ginseng promoted long-term immune memory by increasing the population of memory B cells and cytotoxic T cells in the spleen. In the treatment groups, IgM production was enhanced upon secondary PSV infection.</div></div><div><h3>Conclusions</h3><div>Korean red ginseng modulates immune responses and promotes long-term immunity against low-dose PSV infection. Our data also support the potential of Korean red ginseng as a complementary therapeutic strategy for COVID-19 and an enhancer of vaccine efficacy.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 671-682"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435264","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 : 2025-11-01DOI: 10.1016/j.jgr.2025.06.002
Bin Zhou , Lin Wu , Dinghui Liu , Xiaoying Xie , Ximei Zhang, Yong Liu, Baoshun Hao, Guangyao Shi, Shujie Yu, Zhenda Zheng, Liangying Lin, Min Wang, Xiaoxian Qian
Background
In traditional Chinese medicine ginseng, ginsenoside Rb1 (Rb1) is an active compound that has been shown to alleviate oxidative stress, modulate autophagy, and inhibit apoptosis. However, its role in the natural aging process remains unknown.
Aim
Investigate the role of Rb1 in natural aging and potential molecular mechanisms.
Methods
During eight weeks of treatment with Rb1, we administered low-dose (10 mg/kg·d) or high-dose (20 mg/kg·d) Rb1 to middle-aged (12-month-old) and aged (20-month-old) mice, and observed how changes in body weight and spatial learning were related to aging symptoms. Further, we measured oxidative stress–related markers and nitric oxide (NO) levels in the mice's hippocampal tissue after Rb1 treatment, and identified aging-related biomarkers and pathways.
Results
Treatment with Rb1 greatly reduced the physiological changes associated with aging, such as the weight loss slowing, the inhibition of the loss of visuospatial learning and memory ability, and the senescence of brain tissues. Mice treated with Rb1 had lower serum levels of malondialdehyde (MDA) and higher superoxide dismutase (SOD) activity, along with a reduction in the release of pro-inflammatory markers such tumor necrosis factor-α (TNF-α) and Interleukin-6 (IL-6). Furthermore, Rb1 therapy raised serum NO levels and improved Sirtuin 1 (SIRT1) protein expression, indicating that its anti-aging benefits are connected to the control of the SIRT1/eNOS/NO axis.
Conclusions
Rb1 modulates the SIRT1/eNOS/NO axis, which is linked to reducing oxidative stress and inflammatory reactions, hence delaying the aging process in mice.
{"title":"Ginsenoside Rb1 attenuates age-associated cognitive impairment by modulating oxidative stress and the SIRT1/eNOS/NO axis","authors":"Bin Zhou , Lin Wu , Dinghui Liu , Xiaoying Xie , Ximei Zhang, Yong Liu, Baoshun Hao, Guangyao Shi, Shujie Yu, Zhenda Zheng, Liangying Lin, Min Wang, Xiaoxian Qian","doi":"10.1016/j.jgr.2025.06.002","DOIUrl":"10.1016/j.jgr.2025.06.002","url":null,"abstract":"<div><h3>Background</h3><div>In traditional Chinese medicine ginseng, ginsenoside Rb1 (Rb1) is an active compound that has been shown to alleviate oxidative stress, modulate autophagy, and inhibit apoptosis. However, its role in the natural aging process remains unknown.</div></div><div><h3>Aim</h3><div>Investigate the role of Rb1 in natural aging and potential molecular mechanisms.</div></div><div><h3>Methods</h3><div>During eight weeks of treatment with Rb1, we administered low-dose (10 mg/kg·d) or high-dose (20 mg/kg·d) Rb1 to middle-aged (12-month-old) and aged (20-month-old) mice, and observed how changes in body weight and spatial learning were related to aging symptoms. Further, we measured oxidative stress–related markers and nitric oxide (NO) levels in the mice's hippocampal tissue after Rb1 treatment, and identified aging-related biomarkers and pathways.</div></div><div><h3>Results</h3><div>Treatment with Rb1 greatly reduced the physiological changes associated with aging, such as the weight loss slowing, the inhibition of the loss of visuospatial learning and memory ability, and the senescence of brain tissues. Mice treated with Rb1 had lower serum levels of malondialdehyde (MDA) and higher superoxide dismutase (SOD) activity, along with a reduction in the release of pro-inflammatory markers such tumor necrosis factor-α (TNF-α) and Interleukin-6 (IL-6). Furthermore, Rb1 therapy raised serum NO levels and improved Sirtuin 1 (SIRT1) protein expression, indicating that its anti-aging benefits are connected to the control of the SIRT1/eNOS/NO axis.</div></div><div><h3>Conclusions</h3><div>Rb1 modulates the SIRT1/eNOS/NO axis, which is linked to reducing oxidative stress and inflammatory reactions, hence delaying the aging process in mice.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 6","pages":"Pages 683-691"},"PeriodicalIF":5.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145435265","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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