Journal of Ginseng Research最新文献_第4页

Multi-omics and compositional analysis of bidirectional solid fermentation products from Cordyceps militaris and Panax quinquefolius L 蛹虫草和西洋参双向固体发酵产物的多组学及成分分析

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-09-14 DOI: 10.1016/j.jgr.2025.09.001

Xuan Zhao , Xinrui Li , Xuhui Jia , Yan Gao

Background

Ginsenosides, the main active compounds in American ginseng, have notable pharmacological effects, with rare ginsenosides offering higher bioavailability and bioactivity despite low abundance. Cordyceps militaris, an edible fungus, produces cordycepin and secretes enzymes like β-glucosidase that convert and enhance ginsenoside content. This study employed solid-state fermentation of American ginseng with C. militaris to investigate ginsenoside conversion and enrichment, alongside analyzing changes in cordycepin, gene expression, and metabolites during fermentation.

Materials and methods

In this study, 30 % powdered ginseng was added to the C. militaris culture medium, with samples collected on different days for HPLC analysis of ginsenosides and cordycepin. Transcriptome sequencing and metabolomics analysis of C. militaris was performed on day 40 to investigate the pathways and mechanisms involved in the transformation and enrichment of these components.

Results

HPLC analysis revealed that cordycepin levels in C. militaris cultured with American ginseng increased over time. Rare ginsenoside CK rose from undetectable to 11.81 mg, alongside significant increases in other rare ginsenosides. Mass spectrometry suggests ginsenoside CK is biosynthesized from Rb1 through intermediates Rd and F2. Transcriptome sequencing and metabolomics analysis revealed elevated expression of β-glucosidase and cordycepin synthesis genes. β-glucosidase is involved in carbohydrate and amino acid metabolism pathways, promoting substrate accumulation and providing energy for cordycepin synthesis.

Conclusion

This study demonstrates that co-culture of American ginseng with C. militaris enables bidirectional biotransformation: fungal enzymes convert ginsenosides into rare ginsenosides, while ginseng nutrients upregulate cordycepin biosynthesis. It offers a novel, eco-friendly approach for targeted transformation and enrichment of active ingredients.

人参皂苷是西洋参的主要活性成分，具有显著的药理作用，其含量虽低，但具有较高的生物利用度和生物活性。蛹虫草是一种食用菌，它能产生虫草素，并分泌转化和提高人参皂苷含量的β-葡萄糖苷酶等酶。本研究以西洋参为原料，对西洋参中人参皂苷的转化和富集进行了研究，并分析了发酵过程中虫草素、基因表达和代谢产物的变化。材料与方法本研究将30%的人参粉添加到军蛹虫草培养基中，在不同的日子采集样品，HPLC分析人参皂苷和虫草素的含量。研究人员在第40天对蛹虫草进行转录组测序和代谢组学分析，以探讨这些成分转化和富集的途径和机制。结果hplc分析显示，西洋参培养的蛹虫草素含量随时间的增加而升高。稀有人参皂苷CK从检测不到上升到11.81毫克，与其他稀有人参皂苷显著增加。质谱分析表明，人参皂苷CK是由Rb1通过中间体Rd和F2生物合成的。转录组测序和代谢组学分析显示β-葡萄糖苷酶和虫草素合成基因的表达升高。β-葡萄糖苷酶参与碳水化合物和氨基酸代谢途径，促进底物积累，为虫草素合成提供能量。结论西洋参与军夜蛾共培养可实现双向生物转化：真菌酶可将人参皂苷转化为稀有人参皂苷，而人参营养物质可上调虫草素的生物合成。它提供了一种新颖的、环保的方法，用于有针对性的转化和活性成分的富集。

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引用次数: 0

Ginsenoside Rg3-enriched red ginseng extract mitigates sepsis by inhibiting platelet–leukocyte aggregates and regulates thrombo-inflammatory pathways 人参皂苷rg3富集红参提取物通过抑制血小板-白细胞聚集和调节血栓-炎症途径减轻败血症

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-10-26 DOI: 10.1016/j.jgr.2025.10.006

Yuan Yee Lee , Abdul Wahab Akram , Evelyn Saba , Hyung-Kyu Chae , Min-Goo Seo , Sung Dae Kim , Sang-Joon Park , Dongmi Kwak , Man Hee Rhee

Background

Sepsis is a life-threatening condition characterized by systemic inflammation and thrombo-inflammation, which trigger platelet activation and platelet–leukocyte aggregate (PLA) formation. While Rg3-enriched red ginseng extract (Rg3-RGE) has demonstrated anti-inflammatory and antithrombotic properties, its role in modulating PLAs during sepsis remains poorly understood.

Methods

The in vivo effects of Rg3-RGE were analyzed in a lipopolysaccharide (LPS)-induced murine model of sepsis. Flow cytometry was used to evaluate platelet–leukocyte activation markers. Confocal and scanning electron microscopy (SEM) provided visual evidence of aggregate formation. ELISA was used to quantify plasma levels of tissue factor (TF) and platelet factor 4 (PF4). HPLC analysis revealed the presence of Rb1, Rg3 [20(S) and 20(R)], Rc, Rd, Rf, Rh1, Rb2, and Rg2 [20(S)] in Rg3-RGE. Network pharmacology was employed to identify target interactions and assess their involvement in the thrombo-inflammatory pathway.

Results

Rg3-RGE significantly reduced the activated platelets (CD41+CD62P+), platelet–neutrophil aggregates (PNAs; CD41+Ly6G+), and platelet–monocyte aggregates (PMAs; CD41+CD115+). Confocal imaging confirmed a reduction in PNAs. SEM revealed decreased fibrin-like structures and fewer platelet–leukocyte interactions. Rg3-RGE lowered plasma TF levels, indicating a potential effect on the coagulation cascade, though PF4 levels were not significantly altered. Network pharmacology analysis of ginsenosides in Rg3-RGE identified 235 overlapping targets associated with sepsis, inflammation, platelet activation, and PLA formation. Enrichment analysis revealed key thrombo-inflammatory pathways, including platelet activation, MAPK signaling, PI3K-Akt signaling, sphingosine-1-phosphate receptor signaling, and EGFR signaling.

Conclusion

Rg3-RGE effectively inhibits platelet–leukocyte aggregate formation and mitigates sepsis-induced platelet–leukocyte interactions.

脓毒症是一种危及生命的疾病，其特征是全身炎症和血栓炎症，可触发血小板活化和血小板-白细胞聚集体（PLA）的形成。虽然富含rg3的红参提取物（Rg3-RGE）已被证明具有抗炎和抗血栓的特性，但其在脓毒症期间调节pla的作用仍然知之甚少。方法采用脂多糖（LPS）诱导的脓毒症小鼠模型，观察Rg3-RGE的体内作用。流式细胞术评价血小板-白细胞活化标志物。共聚焦和扫描电子显微镜（SEM）提供了聚集体形成的视觉证据。ELISA法测定血浆组织因子（TF）和血小板因子4 （PF4）水平。HPLC分析显示Rg3- rge中存在Rb1、Rg3 [20(S)和20(R)]， Rc、Rd、Rf、Rh1、Rb2和Rg2 [20(S)]。网络药理学被用来确定目标相互作用，并评估他们参与血栓炎症途径。结果rg3 - rge显著降低活化血小板（CD41+CD62P+）、血小板-中性粒细胞聚集体（PNAs; CD41+Ly6G+）和血小板-单核细胞聚集体（PMAs; CD41+CD115+）。共聚焦成像证实PNAs减少。扫描电镜显示纤维蛋白样结构减少，血小板-白细胞相互作用减少。Rg3-RGE降低了血浆TF水平，表明对凝血级联有潜在影响，但PF4水平没有明显改变。Rg3-RGE中人参皂苷的网络药理学分析发现了235个与脓毒症、炎症、血小板活化和PLA形成相关的重叠靶点。富集分析揭示了关键的血栓炎症通路，包括血小板活化、MAPK信号、PI3K-Akt信号、鞘氨醇-1-磷酸受体信号和EGFR信号。结论rg3 - rge可有效抑制血小板-白细胞聚集形成，减轻败血症诱导的血小板-白细胞相互作用。

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引用次数: 0

Ginsenoside Rg1 attenuates asthma features in mice co-exposed to house dust mite allergen and diesel exhaust particle by modulating epithelial ILC2 interactions 人参皂苷Rg1通过调节上皮ILC2相互作用，减轻了共同暴露于尘螨过敏原和柴油尾气颗粒的小鼠的哮喘特征

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-11-15 DOI: 10.1016/j.jgr.2025.11.007

Hyun Seung Lee , Heung-Woo Park

Background

Airway epithelial cells initiate asthma-related inflammation, making them key therapeutic targets. While some ginsenosides, the principal active constituents of Panax ginseng, are known to modulate epithelial inflammation, the role of ginsenoside Rg1 in this context remains underexplored. This study investigated the therapeutic effects of ginsenoside Rg1 on airway inflammation and airway hyperresponsiveness (AHR) in a murine asthma model induced by co-exposure to Dermatophagoides pteronyssinus (Dp) and diesel exhaust particles (DEP).

Methods

BALB/c mice were exposed intranasally to Dp and DEP with or without ginsenoside Rg1 treatment. AHR, inflammatory cell counts in bronchoalveolar lavage fluid, serum IgG1 levels, lung histopathology, and cytokine levels were assessed. Lung Th2/Th17 cells and ILC2/ILC3 populations were analyzed by flow cytometry. Mechanistic studies were conducted using MLE-12 lung epithelial cells and ILC2 co-cultures.

Results

Co-exposure to Dp and DEP significantly increased AHR, eosinophilic inflammation, Th2/Th17 responses, and ILC2/ILC3 populations. Ginsenoside Rg1 treatment markedly attenuated AHR, reduced eosinophils and serum Dp-specific IgG1, and decreased frequencies of IL-13+ ILC2s and IL-17+ ILC3s. IL-33 and IL-1β levels in lung tissue were also significantly reduced by Rg1. In MLE-12 cells, Rg1 suppressed IL-33 and phosphorylated STAT6 expression, mirroring the effects of a STAT6 inhibitor. Furthermore, Rg1 reduced IL-13 and IL-5 secretion from ILC2s co-cultured with MLE-12 cells.

Conclusion

Ginsenoside Rg1 mitigates Dp/DEP-induced airway inflammation by downregulating Th2/Th17 and ILC2/ILC3 responses, potentially via the IL-33–STAT6 axis in airway epithelial cells.

气道上皮细胞引发哮喘相关炎症，使其成为关键的治疗靶点。虽然一些人参皂苷（人参的主要活性成分）已知可以调节上皮炎症，但人参皂苷Rg1在这种情况下的作用仍未得到充分研究。本研究探讨了人参皂苷Rg1对共暴露于翼状棘球蚴（Dp）和柴油机尾气颗粒（DEP）诱导的小鼠哮喘模型气道炎症和气道高反应性（AHR）的治疗作用。方法balb /c小鼠经鼻暴露于Dp和DEP，并给予或不给予人参皂苷Rg1。评估AHR、支气管肺泡灌洗液炎症细胞计数、血清IgG1水平、肺组织病理学和细胞因子水平。流式细胞术分析肺Th2/Th17细胞和ILC2/ILC3细胞群。使用MLE-12肺上皮细胞和ILC2共培养进行机制研究。结果sco暴露于Dp和DEP显著增加AHR、嗜酸性粒细胞炎症、Th2/Th17反应和ILC2/ILC3群体。人参皂苷Rg1可显著降低AHR，降低嗜酸性粒细胞和血清dp特异性IgG1，降低IL-13+ ILC2s和IL-17+ ILC3s的频率。肺组织IL-33和IL-1β水平也显著降低。在MLE-12细胞中，Rg1抑制IL-33并磷酸化STAT6的表达，反映了STAT6抑制剂的作用。此外，Rg1降低了与MLE-12细胞共培养的ILC2s分泌IL-13和IL-5。结论人参皂苷Rg1通过下调气道上皮细胞的Th2/Th17和ILC2/ILC3反应，可能通过IL-33-STAT6轴减轻Dp/ dep诱导的气道炎症。

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引用次数: 0

Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling 生物转化野生人参的肾保护机制：通过Nrf2/HO-1/NF-κB/caspase-3信号通路减轻氧化应激、炎症和细胞凋亡对缺血性肾损伤的保护作用

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-10-26 DOI: 10.1016/j.jgr.2025.10.007

Ye Ji Kim , Md Shiblee Sadik Sabuj , Myung-Kon Kim , Joonseok Lee , Ryunhee Kim , Seung Hyun Lee , Jin Min Oh , Hyeon Gyeong Ro , In-Shik Kim , Dongchoon Ahn , Md Rashedunnabi Akanda , Hyun-Jin Tae , Byung-Yong Park

Background

Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is a severe condition linked to higher morbidity and mortality. Panax ginseng (PG) possesses renoprotective properties; however, its inadequate bioavailability restricts its efficacy. Wild-simulated PG (WSG), processed to boost its bioactive components, exhibits improved renoprotective effects. This research examines PG, bioconverted PG (BPG), and bioconverted WSG (BWG) for their protective roles against I/R induced AKI in mice.

Methods

C57BL/6 mice underwent bilateral renal pedicle clamping via a dorsal approach for 30 min to induce ischemia, followed by clamp release and 24 h of reperfusion. Blood and kidney samples were collected at the end of the reperfusion period. Sham-operated mice underwent identical procedures without vascular clamping. Additionally, hydrogen peroxide (H₂O₂) induced oxidative stress in HK-2 cells.

Results

The effects of each extract were evaluated. Expression of antioxidant, inflammatory, and apoptotic factors was confirmed using western blotting, immunohistochemistry, and TUNEL assays. Both extracts improved the survival of H₂O₂-treated HK-2 cells and enhanced kidney function, as indicated by reduced BUN and Cr levels. Histopathological analysis showed decreased injury, preserved tubular structure, and reduced inflammation in extract-treated groups. These protective effects were linked to activation of the Nrf2/HO-1 pathway, leading to increased expression of antioxidant enzymes (CAT, GPX-1, SOD-1) and reduced malondialdehyde (MDA) levels. Moreover, the extracts downregulated pro-inflammatory cytokines (TNF-α, IL-1β), suppressed NF-κB phosphorylation, decreased Bax/Bcl-2 ratio and Caspase-3 activation, enhancing cell survival.

Conclusion

BPG and BWG remarkably ameliorated I/R-induced AKI through modulation of Nrf2/HO-1/NF-κB/Caspase-3 signaling pathway, with BWG exhibiting more substantial renoprotective effects.

缺血再灌注（I/R）引起的急性肾损伤（AKI）是一种与高发病率和死亡率相关的严重疾病。人参具有保护肾的作用；然而，其生物利用度不足限制了其疗效。野生模拟PG (WSG)，加工以提高其生物活性成分，表现出改善的肾保护作用。本研究探讨了PG、生物转化PG （BPG）和生物转化WSG （BWG）对I/R诱导小鼠AKI的保护作用。方法sc57bl /6小鼠经背侧入路双侧肾蒂夹持30 min诱导缺血，然后释放夹持，再灌注24 h。在再灌注期结束时采集血液和肾脏标本。假手术小鼠在没有血管夹紧的情况下进行相同的手术。此外，过氧化氢（H2O2）诱导HK-2细胞氧化应激。结果对各提取物的作用进行了评价。western blotting、免疫组织化学和TUNEL检测证实了抗氧化、炎症和凋亡因子的表达。两种提取物均能提高h2o2处理的HK-2细胞的存活率，并通过降低BUN和Cr水平来增强肾功能。组织病理学分析显示，提取物组损伤减轻，保留了管状结构，炎症减轻。这些保护作用与Nrf2/HO-1通路的激活有关，导致抗氧化酶（CAT、GPX-1、SOD-1）的表达增加，丙二醛（MDA）水平降低。此外，提取物下调促炎因子（TNF-α、IL-1β），抑制NF-κB磷酸化，降低Bax/Bcl-2比值和Caspase-3活性，提高细胞存活率。结论bpg和BWG通过调节Nrf2/HO-1/NF-κB/Caspase-3信号通路显著改善I/ r诱导的AKI， BWG表现出更明显的肾保护作用。

{"title":"Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling","authors":"Ye Ji Kim , Md Shiblee Sadik Sabuj , Myung-Kon Kim , Joonseok Lee , Ryunhee Kim , Seung Hyun Lee , Jin Min Oh , Hyeon Gyeong Ro , In-Shik Kim , Dongchoon Ahn , Md Rashedunnabi Akanda , Hyun-Jin Tae , Byung-Yong Park","doi":"10.1016/j.jgr.2025.10.007","DOIUrl":"10.1016/j.jgr.2025.10.007","url":null,"abstract":"<div><h3>Background</h3><div>Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is a severe condition linked to higher morbidity and mortality. <em>Panax ginseng</em> (PG) possesses renoprotective properties; however, its inadequate bioavailability restricts its efficacy. Wild-simulated PG (WSG), processed to boost its bioactive components, exhibits improved renoprotective effects. This research examines PG, bioconverted PG (BPG), and bioconverted WSG (BWG) for their protective roles against I/R induced AKI in mice.</div></div><div><h3>Methods</h3><div>C57BL/6 mice underwent bilateral renal pedicle clamping via a dorsal approach for 30 min to induce ischemia, followed by clamp release and 24 h of reperfusion. Blood and kidney samples were collected at the end of the reperfusion period. Sham-operated mice underwent identical procedures without vascular clamping. Additionally, hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) induced oxidative stress in HK-2 cells.</div></div><div><h3>Results</h3><div>The effects of each extract were evaluated. Expression of antioxidant, inflammatory, and apoptotic factors was confirmed using western blotting, immunohistochemistry, and TUNEL assays. Both extracts improved the survival of H<sub>2</sub>O<sub>2</sub>-treated HK-2 cells and enhanced kidney function, as indicated by reduced BUN and Cr levels. Histopathological analysis showed decreased injury, preserved tubular structure, and reduced inflammation in extract-treated groups. These protective effects were linked to activation of the Nrf2/HO-1 pathway, leading to increased expression of antioxidant enzymes (CAT, GPX-1, SOD-1) and reduced malondialdehyde (MDA) levels. Moreover, the extracts downregulated pro-inflammatory cytokines (TNF-α, IL-1β), suppressed NF-κB phosphorylation, decreased Bax/Bcl-2 ratio and Caspase-3 activation, enhancing cell survival.</div></div><div><h3>Conclusion</h3><div>BPG and BWG remarkably ameliorated I/R-induced AKI through modulation of Nrf2/HO-1/NF-κB/Caspase-3 signaling pathway, with BWG exhibiting more substantial renoprotective effects.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100910"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ginsenoside Re mitigates Aβ1-42-induced neurotoxicity by promoting autophagy and suppressing NLRP3 inflammasome 人参皂苷Re通过促进自噬和抑制NLRP3炎性体减轻a β1-42诱导的神经毒性

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-10-31 DOI: 10.1016/j.jgr.2025.10.008

Iskander Madhi, Ji-Hee Kim, Hyun Seung Shin, Yun Hee So, Eui-Man Jung, YoungHee Kim

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) accumulation and neuroinflammation. Activation of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome in microglia significantly contributes to AD-associated neuroinflammation and neuronal damage. Ginsenoside Re (G-Re), a major bioactive constituent of Panax ginseng, exhibits anti-inflammatory properties, but its role in modulating inflammasome activation in AD remains unclear.

Methods

This study evaluated the therapeutic potential of G-Re in mice intracerebroventricularly injected with Aβ_1-42 and delineated its molecular mechanisms in complementary cell-based models. We employed behavioral testing, immunohistochemistry, Western blotting, enzyme-linked immunosorbent assays, Annexin V apoptosis assays, and mitochondrial functional assays.

Results

Intraperitoneal administration of G-Re significantly improved cognitive performance, as evidenced by enhanced outcomes in the T-maze and novel object recognition tests. G-Re treatment reduced microglial activation and interleukin-1β (IL-1β) levels in the cortex and hippocampus. In vitro, G-Re protected neurons from conditioned medium derived from Aβ_1-42-stimulated microglia, showing neuroprotection comparable to anti-IL-1β treatment. G-Re also inhibited Aβ_1-42-induced activation of the NLRP3 inflammasome, as indicated by diminished levels of NLRP3, cleaved caspase-1, cleaved gasdermin D (GSDMD), IL-1β, and IL-18 in brain tissues and cultured microglia. Mechanistically, G-Re reduced mitochondrial reactive oxygen species (mtROS), preserved mitochondrial membrane potential, and activated autophagy via SIRT1/AMPK/mTOR signaling, thereby suppressing inflammasome activation.

Conclusion

G-Re ameliorates Aβ_1-42-induced neuroinflammation and cognitive impairment by restoring mitochondrial homeostasis, enhancing autophagy, and suppressing NLRP3 inflammasome activation. These findings suggest G-Re as a potential therapeutic intervention for neurodegenerative disorders including AD.

阿尔茨海默病（AD）是一种以β-淀粉样蛋白（a β）积累和神经炎症为特征的进行性神经退行性疾病。小胶质细胞中nod样受体pyrin结构域3 （NLRP3）炎性小体的激活可显著促进ad相关的神经炎症和神经元损伤。人参皂苷Re （G-Re）是人参的主要生物活性成分，具有抗炎特性，但其在AD中调节炎性体激活的作用尚不清楚。方法本研究评价了Aβ1-42对小鼠脑室注射G-Re的治疗潜力，并在互补细胞模型中描述了其分子机制。我们采用了行为测试、免疫组织化学、免疫印迹、酶联免疫吸附测定、膜联蛋白V凋亡测定和线粒体功能测定。结果经腹腔注射G-Re可显著改善大鼠的认知能力，t迷宫和新物体识别测试的结果均有所提高。G-Re治疗降低了皮质和海马的小胶质细胞活化和白细胞介素-1β (IL-1β)水平。在体外，G-Re保护来自a β1-42刺激的小胶质细胞的条件培养基中的神经元，显示出与抗il -1β治疗相当的神经保护作用。G-Re还抑制了a β1-42诱导的NLRP3炎性体的激活，脑组织和培养的小胶质细胞中NLRP3、cleaved caspase-1、cleaved gasdermin D （GSDMD）、IL-1β和IL-18的水平降低。从机制上说，G-Re减少线粒体活性氧（mtROS），保存线粒体膜电位，并通过SIRT1/AMPK/mTOR信号激活自噬，从而抑制炎症小体的激活。结论- re可通过恢复线粒体稳态、增强自噬、抑制NLRP3炎性体激活等途径改善a β1-42诱导的神经炎症和认知功能障碍。这些发现表明G-Re是包括AD在内的神经退行性疾病的潜在治疗干预手段。

{"title":"Ginsenoside Re mitigates Aβ1-42-induced neurotoxicity by promoting autophagy and suppressing NLRP3 inflammasome","authors":"Iskander Madhi, Ji-Hee Kim, Hyun Seung Shin, Yun Hee So, Eui-Man Jung, YoungHee Kim","doi":"10.1016/j.jgr.2025.10.008","DOIUrl":"10.1016/j.jgr.2025.10.008","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) accumulation and neuroinflammation. Activation of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome in microglia significantly contributes to AD-associated neuroinflammation and neuronal damage. Ginsenoside Re (G-Re), a major bioactive constituent of <em>Panax ginseng</em>, exhibits anti-inflammatory properties, but its role in modulating inflammasome activation in AD remains unclear.</div></div><div><h3>Methods</h3><div>This study evaluated the therapeutic potential of G-Re in mice intracerebroventricularly injected with Aβ<sub>1-42</sub> and delineated its molecular mechanisms in complementary cell-based models. We employed behavioral testing, immunohistochemistry, Western blotting, enzyme-linked immunosorbent assays, Annexin V apoptosis assays, and mitochondrial functional assays.</div></div><div><h3>Results</h3><div>Intraperitoneal administration of G-Re significantly improved cognitive performance, as evidenced by enhanced outcomes in the T-maze and novel object recognition tests. G-Re treatment reduced microglial activation and interleukin-1β (IL-1β) levels in the cortex and hippocampus. In vitro, G-Re protected neurons from conditioned medium derived from Aβ<sub>1-42</sub>-stimulated microglia, showing neuroprotection comparable to anti-IL-1β treatment. G-Re also inhibited Aβ<sub>1-42</sub>-induced activation of the NLRP3 inflammasome, as indicated by diminished levels of NLRP3, cleaved caspase-1, cleaved gasdermin D (GSDMD), IL-1β, and IL-18 in brain tissues and cultured microglia. Mechanistically, G-Re reduced mitochondrial reactive oxygen species (mtROS), preserved mitochondrial membrane potential, and activated autophagy via SIRT1/AMPK/mTOR signaling, thereby suppressing inflammasome activation.</div></div><div><h3>Conclusion</h3><div>G-Re ameliorates Aβ<sub>1-42</sub>-induced neuroinflammation and cognitive impairment by restoring mitochondrial homeostasis, enhancing autophagy, and suppressing NLRP3 inflammasome activation. These findings suggest G-Re as a potential therapeutic intervention for neurodegenerative disorders including AD.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100911"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877030","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}

引用次数: 0

Ginsenoside Rb1 restores dental pulp by promoting odontogenic differentiation of dental pulp stem cells via the TGF-β/Smad signaling pathway 人参皂苷Rb1通过TGF-β/Smad信号通路促进牙髓干细胞成牙分化，从而修复牙髓

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-11-06 DOI: 10.1016/j.jgr.2025.11.001

Ok Hyung Nam , Seong Eun Kim , Si Won Kang , Hyekyoung You , Myeong-Kwan Jih , Jaeyoung Ryu , Young Kim

Background

Dental surgery is a common treatment for pulpitis, which can lead to decreased pulp vitality. A novel approach is needed to induce reparative dentin formation without pulp removal. Ginsenoside Rb1 (G-Rb1) is known for its regenerative properties in various diseases. This study aimed to examine the odontogenic differentiation-promoting effects of G-Rb1 in human dental pulp stem cells (hDPSCs) and a rat pulpotomy model, and explore the underlying molecular mechanisms.

Methods

hDPSCs were extracted from supernumerary teeth and cultured with 10 μg/mL G-Rb1. Odontoblastic differentiation was assessed through real-time PCR, western blot, ALP activity, and Alizarin Red S staining. RNA sequencing was performed to confirm the effects of G-Rb1 on odontogenesis of hDPSCs. The effects in the rat pulpotomy model were evaluated by examining reparative dentin formation using von Kossa staining.

Results

G-Rb1 was non-cytotoxic and significantly enhanced hDPSC migration and odontoblastic differentiation in hDPSCs, upregulating the expression of odontogenic markers, DMP1 and DSPP, and increasing mineralized nodule deposition. RNA sequencing identified the TGF-β/Smad pathway as a key mechanism underlying these effects, which was confirmed by evaluating the expression of pathway-related proteins. In vivo analysis demonstrated significantly higher reparative dentin formation in the G-Rb1-treated group compared to the control group.

Conclusion

G-Rb1 promotes odontoblastic differentiation in hDPSCs and enhances reparative dentin formation via the TGF-β/Smad signaling pathway. These findings highlight the potential of G-Rb1 as a therapeutic agent for dental pulp repair and regeneration.

牙髓手术是治疗牙髓炎的常用方法，可导致牙髓活力下降。需要一种新的方法来诱导修复性牙本质的形成而不需要去除牙髓。人参皂苷Rb1 （G-Rb1）因其在多种疾病中的再生特性而闻名。本研究旨在探讨G-Rb1在人牙髓干细胞（hDPSCs）和大鼠断牙模型中促进成牙分化的作用，并探讨其分子机制。方法用10 μg/mL G-Rb1培养多牙dpscs。通过实时荧光定量PCR、western blot、ALP活性和茜素红S染色评估成牙细胞分化。通过RNA测序证实G-Rb1对hdpsc成牙发育的影响。von Kossa染色法观察修复性牙本质形成，评价其对大鼠断髓模型的影响。结果g - rb1无细胞毒性，可显著增强hDPSC在hDPSC中的迁移和成牙细胞分化，上调成牙标志物DMP1和DSPP的表达，增加矿化结节沉积。RNA测序发现TGF-β/Smad通路是这些作用的关键机制，通过评估通路相关蛋白的表达证实了这一点。体内分析表明，与对照组相比，g - rb1处理组的修复性牙本质形成显著增加。结论- rb1通过TGF-β/Smad信号通路促进hDPSCs成牙细胞分化，促进修复性牙本质形成。这些发现突出了G-Rb1作为牙髓修复和再生治疗剂的潜力。

{"title":"Ginsenoside Rb1 restores dental pulp by promoting odontogenic differentiation of dental pulp stem cells via the TGF-β/Smad signaling pathway","authors":"Ok Hyung Nam , Seong Eun Kim , Si Won Kang , Hyekyoung You , Myeong-Kwan Jih , Jaeyoung Ryu , Young Kim","doi":"10.1016/j.jgr.2025.11.001","DOIUrl":"10.1016/j.jgr.2025.11.001","url":null,"abstract":"<div><h3>Background</h3><div>Dental surgery is a common treatment for pulpitis, which can lead to decreased pulp vitality. A novel approach is needed to induce reparative dentin formation without pulp removal. Ginsenoside Rb1 (G-Rb1) is known for its regenerative properties in various diseases. This study aimed to examine the odontogenic differentiation-promoting effects of G-Rb1 in human dental pulp stem cells (hDPSCs) and a rat pulpotomy model, and explore the underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>hDPSCs were extracted from supernumerary teeth and cultured with 10 μg/mL G-Rb1. Odontoblastic differentiation was assessed through real-time PCR, western blot, ALP activity, and Alizarin Red S staining. RNA sequencing was performed to confirm the effects of G-Rb1 on odontogenesis of hDPSCs. The effects in the rat pulpotomy model were evaluated by examining reparative dentin formation using von Kossa staining.</div></div><div><h3>Results</h3><div>G-Rb1 was non-cytotoxic and significantly enhanced hDPSC migration and odontoblastic differentiation in hDPSCs, upregulating the expression of odontogenic markers, DMP1 and DSPP, and increasing mineralized nodule deposition. RNA sequencing identified the TGF-β/Smad pathway as a key mechanism underlying these effects, which was confirmed by evaluating the expression of pathway-related proteins. <em>In vivo</em> analysis demonstrated significantly higher reparative dentin formation in the G-Rb1-treated group compared to the control group.</div></div><div><h3>Conclusion</h3><div>G-Rb1 promotes odontoblastic differentiation in hDPSCs and enhances reparative dentin formation via the TGF-β/Smad signaling pathway. These findings highlight the potential of G-Rb1 as a therapeutic agent for dental pulp repair and regeneration.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"50 1","pages":"Article 100913"},"PeriodicalIF":5.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877031","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}

引用次数: 0

Effects of Korean red ginseng on the HIV-1 env sequence length and CpG dinucleotides 红参对HIV-1 env序列长度和CpG二核苷酸的影响

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-11-08 DOI: 10.1016/j.jgr.2025.11.004

Jinny Lee , Seunghee Baek , Young-Keol Cho

Background

Korean Red Ginseng (KRG) and KRG combination therapies have demonstrated long-term benefits in HIV-1-infected patients. This study aimed to assess whether long-term KRG treatment influences sequence length (SL) and CpG700 content in the HIV-1 env gene.

Materials and methods

880 wild-type, full-length env gene sequences were obtained from 482 samples via nested PCR or RT-PCR over a mean duration of 8.0 ± 8.0 years in 200 HIV-1-infected patients. SL and CpG700 content were compared between KRG-naïve (KN, n = 97) and KRG-experienced (KE, n = 103) patients at the time of sequencing, including during the antiretroviral therapy (ART) period. The number of patients with 1, 2, 3 and ≥4 sequenced interval samples was 113, 34, 15, and 38, respectively.

Results

In the whole cohort, the correlation between SL and disease duration (DD) from diagnosis, both before and during ART, was significantly stronger in KE patients than in KN patients (P < 0.01), whereas CpG700 showed no such correlation with DD or KRG. To reduce selection bias, we further analyzed only patients with two or more samples sequenced samples; in this subgroup, both SL and CpG700 demonstrated significant correlations with DD and KRG, with correlation strength increasing as follow-up duration increased. Notably, in the high-intake group receiving prolonged, intensive KRG treatment, CpG700 correlated more strongly with KRG than with DD or SL.

Conclusion

Env SL and CpG700 content are significantly associated with KRG treatment, with the association between KRG and CpG700 becoming more evident over longer follow-up.

韩国红参（KRG）和KRG联合治疗已证明对hiv -1感染患者有长期益处。本研究旨在评估长期KRG治疗是否会影响HIV-1 env基因的序列长度（SL）和CpG700含量。材料与方法从200例hiv -1感染者的482份样本中，通过巢式PCR或RT-PCR获得880个野生型、全长env基因序列，平均持续时间为8.0±8.0年。在测序时比较KRG-naïve （KN, n = 97）和krg经历（KE, n = 103）患者的SL和CpG700含量，包括抗逆转录病毒治疗（ART）期间。有1、2、3和≥4个测序间隔样本的患者分别为113、34、15和38例。结果在整个队列中，KE患者在ART前和ART期间的SL与疾病病程（DD）的相关性显著强于KN患者（P < 0.01），而CpG700与DD或KRG均无相关性。为了减少选择偏差，我们进一步只分析有两个或两个以上样本的患者；在该亚组中，SL和CpG700与DD和KRG均表现出显著的相关性，且随随访时间的增加，相关性增强。值得注意的是，在接受长期强化KRG治疗的高摄入量组中，CpG700与KRG的相关性比与DD或SL的相关性更强。结论env SL和CpG700含量与KRG治疗显著相关，随着随访时间的延长，KRG和CpG700的相关性变得更加明显。

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引用次数: 0

The role of ginseng and ginsenosides in ROS and cardiovascular disease 人参及其皂苷在活性氧和心血管疾病中的作用

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2026-01-01 Epub Date: 2025-09-02 DOI: 10.1016/j.jgr.2025.08.008

Ajay Vijayakumar, Jun Hong Park, Jong-Hoon Kim

An imbalance in reactive oxygen species (ROS) can lead to severe tissue damage and ultimately result in cell death. While ROS plays a crucial role in cellular signaling, excessive ROS production disrupts intracellular homeostasis, causing oxidative stress, which is a contributing factor to cardiac diseases. Ginseng and its ginsenosides have demonstrated potent antioxidant and cardioprotective properties, and their effectiveness in combating oxidative stress which is closely associated with cardiac health has been thoroughly documented. This review summarizes the cardioprotective roles and molecular mechanisms through which ginseng and its key and rare ginsenosides regulate excess ROS production, restore antioxidant enzyme function, and ameliorate cardiac damage. Key ginsenosides such as Rg1, Rg3, Rb1, and notoginsenoside R1, along with rare forms like Rh1, Rh4, F₂, Mc-1, and TP1 exhibit anti-oxidative property and promote cardiac recovery through both well-established and novel signaling pathways. Recent advances and emerging clinical trial data suggest potential benefits in conditions such as hypertension, ischemia, cardiotoxicity and vascular dysfunction. Collectively, these findings highlight the significance of ginseng and its ginsenoside as valuable adjunct therapy in modern cardiovascular treatment. Further clinical exploration could help translate these preclinical findings into effective cardiac therapies.

活性氧（ROS）失衡可导致严重的组织损伤并最终导致细胞死亡。虽然ROS在细胞信号传导中起着至关重要的作用，但过量的ROS产生会破坏细胞内稳态，引起氧化应激，这是导致心脏病的一个因素。人参及其皂苷已被证明具有有效的抗氧化和保护心脏的特性，它们在对抗与心脏健康密切相关的氧化应激方面的有效性已被充分证明。本文就人参及其关键和稀有人参皂苷调节活性氧过剩、恢复抗氧化酶功能、改善心脏损伤的保护作用及其分子机制进行综述。关键人参皂苷如Rg1、Rg3、Rb1和三七皂苷R1，以及罕见的形式如Rh1、Rh4、F2、Mc-1和TP1表现出抗氧化特性，并通过建立和新的信号通路促进心脏恢复。最近的进展和新出现的临床试验数据表明，它对高血压、缺血、心脏毒性和血管功能障碍等疾病有潜在的益处。总的来说，这些发现突出了人参及其人参皂苷在现代心血管治疗中作为有价值的辅助疗法的意义。进一步的临床探索可能有助于将这些临床前发现转化为有效的心脏治疗方法。

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引用次数: 0

Ginsenoside Rc mitigates hippocampal neuronal damage and cognitive impairment in vascular dementia rats via the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways 人参皂苷Rc通过pY705-Stat3/Foxo3a和pS727-Stat3/GRIM-19通路减轻血管性痴呆大鼠海马神经元损伤和认知功能障碍

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 Epub Date: 2025-07-24 DOI: 10.1016/j.jgr.2025.07.003

Yuying Wu , Zhizhen Zhang , Xiaoyuan Lian

Background

Vascular dementia (VaD), the second most common cause of dementia, lacks effective treatments. Ginsenoside Rc (GRc) has demonstrated therapeutic potential, but its role in VaD remains unclear. This study investigates the protective effects of GRc in VaD and its underlying mechanisms.

Methods

Cognitive function was assessed using novel object recognition and Morris water maze tests. Neuronal and glial status in the cortex and hippocampus were evaluated by immunohistochemistry, Nissl staining, immunofluorescence, transmission electron microscopy, and Western blotting. Drug target identification was performed through molecular docking, molecular dynamics simulations, and cellular thermal shift assay. Apoptosis markers, along with pY705-Stat3/Foxo3a/Nrf2 and pS727-Stat3/GRIM-19/Sirt1/PGC1α pathway-related factors, were analyzed by cell viability assay, Western blotting, immunoprecipitation, and commercial assay kits.

Results

GRc ameliorated cognitive deficits in VaD rats, attenuating synaptic disruption and neuronal apoptosis in the hippocampal CA1 region. GRc bound to Stat3 and promoted its phosphorylation at Y705 and S727. It further enhanced catalase and SOD activity through pY705-Stat3-mediated Foxo3a activation and upregulated GSR, Gpx4, and GSH via the Nrf2 pathway. Moreover, GRc stabilized the pS727-Stat3/GRIM-19 complex, facilitating mitochondrial translocation of pS727-Stat3, which enhanced mitochondrial Complex I and II activities, increased NAD⁺ levels, and activated the Sirt1/PGC1α pathway, promoting mitochondrial biogenesis and ATP production.

Conclusion

GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. Through the pY705-Stat3/Foxo3a and pS727-Stat3/GRIM-19 pathways, GRc alleviated hippocampal neuronal apoptosis and synaptic dysfunction, thereby improving cognitive function in VaD rats.

背景：血管性痴呆（VaD）是痴呆症的第二大常见原因，缺乏有效的治疗方法。人参皂苷Rc （GRc）已显示出治疗潜力，但其在VaD中的作用尚不清楚。本研究探讨GRc对VaD的保护作用及其潜在机制。方法采用新颖的物体识别和Morris水迷宫测试对认知功能进行评估。通过免疫组织化学、尼氏染色、免疫荧光、透射电镜和Western blotting评估皮层和海马的神经元和胶质状态。通过分子对接、分子动力学模拟和细胞热移实验进行药物靶标鉴定。细胞凋亡标志物以及pY705-Stat3/Foxo3a/Nrf2和pS727-Stat3/GRIM-19/Sirt1/PGC1α通路相关因子通过细胞活力测定、Western blotting、免疫沉淀和商用检测试剂盒进行分析。结果grc可改善VaD大鼠的认知缺陷，减轻海马CA1区突触破坏和神经元凋亡。GRc结合Stat3并促进其Y705和S727位点的磷酸化。它通过py705 - stat3介导的Foxo3a激活进一步增强过氧化氢酶和SOD活性，并通过Nrf2途径上调GSR、Gpx4和GSH。此外，GRc稳定了pS727-Stat3/GRIM-19复合体，促进了pS727-Stat3的线粒体易位，从而增强了线粒体复合体I和II的活性，增加了NAD+水平，激活了Sirt1/PGC1α通路，促进了线粒体的生物发生和ATP的产生。结论grc通过靶向Stat3并驱动其双磷酸化发挥VaD的神经保护作用。GRc通过pY705-Stat3/Foxo3a和pS727-Stat3/GRIM-19通路，减轻VaD大鼠海马神经元凋亡和突触功能障碍，从而改善VaD大鼠认知功能。

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引用次数: 0

Pharmacokinetics and pharmacological activities of protopanaxatriol 原多巴胺醇的药代动力学及药理活性

IF 5.6 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-11-01 Epub Date: 2025-08-06 DOI: 10.1016/j.jgr.2025.07.004

Yeye Hu , Jae Youl Cho , Mi-Yeon Kim

Protopanaxatriol (PPT) is an active metabolite derived from protopanaxatriol-type ginsenosides from Panax ginseng, displaying broad range of pharmacological activities against various diseases with higher efficacy. Since ginsenosides are known to be active components from ginseng, exploring biological activities and functions of the components could be important in terms of understanding ginseng's pharmacological roles. In this review, we aimed to report biological role of PPT by analyzing published literatures and databases. For this purpose, pharmacokinetics and pharmacological activities of PPT, including cardiovascular protection; neuroprotection; skin protection; immunomodulation; and anti-cancer, anti-inflammatory, and anti-diabetes effects were focused. In addition, we also discuss the underlying pharmacological mechanisms of action. This review highlights the importance of PPT for its overall efficacy and aims to inspire further exploration of its diverse potential applications.

原人参醇（PPT）是从人参中提取的一种活性代谢物，对多种疾病具有广泛的药理活性，疗效较高。由于人参皂苷是人参的有效成分，探索人参皂苷的生物活性和功能对了解人参的药理作用具有重要意义。在这篇综述中，我们旨在通过分析已发表的文献和数据库来报道PPT的生物学作用。为此，研究PPT的药代动力学和药理活性，包括心血管保护作用；神经保护;皮肤保护;免疫调节;重点研究了抗癌、抗炎和抗糖尿病的效果。此外，我们还讨论了潜在的药理作用机制。本文综述了PPT在整体疗效方面的重要性，旨在启发进一步探索PPT的多种潜在应用。

引用次数: 0