Journal of Ginseng Research最新文献_第9页

Ginsenoside Rc prevents dexamethasone-induced muscle atrophy and enhances muscle strength and motor function 人参皂苷 Rc 可防止地塞米松诱发的肌肉萎缩，增强肌肉力量和运动功能

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-01-01 DOI: 10.1016/j.jgr.2024.09.002

Aeyung Kim , Sang-Min Park , No Soo Kim , Musun Park , Seongwon Cha

Background

A decline in muscle mass and function can impact the health, disease vulnerability, and mortality of older adults. Prolonged use of high doses of glucocorticoids, such as dexamethasone (DEX), can cause muscle wasting and reduced strength. Ginsenoside Rc (gRc) has been shown to protect muscles by activating the PGC-1α pathway and improving mitochondrial function. The effects of gRc on muscle atrophy and function in mice are not fully understood.

Methods and results

The study discovered that gRc prevented the DEX-induced decrease in viability of C2C12 myoblasts and myotubes. Furthermore, gRc inhibited myotube degradation and the upregulation of muscle degradation proteins induced by DEX. Transcriptome analysis of myotubes showed that gRc enhances muscle generation processes while suppressing the TGF-β pathway and oxidative stress response. In mice, gRc effectively reversed the reductions in body weight, muscle mass, and muscle fibers caused by DEX. Furthermore, gRc significantly enhanced muscle strength and exercise capacity. Docking and transcriptome analyses indicated that gRc may act as a competitive inhibitor of DEX at the glucocorticoid receptor, potentially preventing muscle loss.

Conclusion

The study suggests that gRc can prevent DEX-induced muscle wasting and weakness. Consequently, it may be a viable treatment option for sarcopenia and muscle-related disorders in various medical conditions.

肌肉质量和功能的下降会影响老年人的健康、疾病易感性和死亡率。长期使用大剂量糖皮质激素，如地塞米松（DEX），会导致肌肉萎缩和力量下降。研究表明，人参皂苷 Rc（gRc）可通过激活 PGC-1α 通路和改善线粒体功能来保护肌肉。目前还不完全清楚人参皂苷 Rc 对小鼠肌肉萎缩和功能的影响。研究发现，gRc能防止DEX诱导的C2C12成肌细胞和肌管活力下降。此外，gRc还能抑制DEX诱导的肌管降解和肌肉降解蛋白的上调。肌细胞的转录组分析表明，gRc在抑制TGF-β途径和氧化应激反应的同时，还能增强肌肉的生成过程。在小鼠体内，gRc能有效逆转DEX导致的体重、肌肉质量和肌肉纤维的减少。此外，gRc 还能明显增强肌肉力量和运动能力。对接和转录组分析表明，gRc可能是DEX在糖皮质激素受体上的竞争性抑制剂，有可能防止肌肉流失。这项研究表明，gRc 可以防止 DEX 引起的肌肉萎缩和虚弱。因此，它可能是治疗各种病症中肌肉疏松症和肌肉相关疾病的一种可行方法。

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引用次数: 0

Ginsenoside Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through TXNIP/NLRP3 pathway-modulated mitophagy 人参皂苷Rg1通过TXNIP/NLRP3通路调节的线粒体自噬改善缺氧诱导的肺血管内皮功能障碍。

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-01-01 DOI: 10.1016/j.jgr.2024.10.002

Ru Zhang, Meili Lu, Chenyang Ran, Linchao Niu, Qi Qi, Hongxin Wang

Background

Vascular endothelial dysfunction (VED) is one of the main pathogenic events in pulmonary arterial hypertension (PAH). Previous studies have demonstrated that the ginsenoside Rg1 (Rg1) can ameliorate PAH, but the mechanism by which Rg1 affects pulmonary VED in hypoxia-induced PAH remains unclear.

Methods

Network pharmacology, molecular docking and other experiments were used to explore the mechanisms by which Rg1 affects PAH. A PAH mouse model was established via hypoxia combined with the vascular endothelial growth factor (VEGFR) inhibitor su5416 (SuHx), and a cell model was established via hypoxia. The functions of Rg1 in VED, oxidative stress, inflammation, mitophagy, and TXNIP and NLRP3 expression were examined.

Results

In hypoxia-induced VED, progressive exacerbation of oxidative stress, inflammation, and mitophagy were observed, and were associated with elevated TXNIP and NLRP3 expression in vivo and in vitro. Rg1 improved hypoxia-induced impaired endothelium-dependent vasodilation and increased nitric oxide (NO) and endothelial NO synthase (eNOS) expression. Rg1, SRI37330 (a TXNIP inhibitor), MCC950 (an NLRP3 inhibitor), and Liensinine (a mitophagy inhibitor) attenuated oxidative stress, inflammation, and mitophagy by reducing the expression of TXNIP and NLRP3 in mice and cells. Furthermore, the combination of SB203580 (a mitophagy agonist) with Rg1 disrupted the protective effect of Rg1 on hypoxia-induced pulmonary artery and human pulmonary artery endothelial cells (HPAECs).

Conclusion

Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through TXNIP/NLRP3 pathway-modulated oxidative stress, inflammation and mitophagy.

背景：血管内皮功能障碍（VED）是肺动脉高压（PAH）的主要致病事件之一。先前的研究表明人参皂苷Rg1 （Rg1）可以改善PAH，但Rg1在缺氧诱导的PAH中影响肺部VED的机制尚不清楚。方法：通过网络药理学、分子对接等实验，探讨Rg1影响PAH的机制。通过缺氧联合血管内皮生长因子（VEGFR）抑制剂su5416 （SuHx）建立PAH小鼠模型，通过缺氧建立细胞模型。检测Rg1在VED、氧化应激、炎症、线粒体自噬以及TXNIP和NLRP3表达中的功能。结果：在缺氧诱导的VED中，观察到氧化应激、炎症和线粒体自噬的进行性加重，并与体内和体外TXNIP和NLRP3表达升高有关。Rg1改善缺氧诱导的内皮依赖性血管舒张功能受损，增加一氧化氮（NO）和内皮NO合成酶（eNOS）表达。Rg1、SRI37330 （TXNIP抑制剂）、MCC950 （NLRP3抑制剂）和Liensinine（线粒体自噬抑制剂）通过降低小鼠和细胞中TXNIP和NLRP3的表达来减轻氧化应激、炎症和线粒体自噬。此外，SB203580（一种线粒体自噬激动剂）与Rg1联合使用可破坏Rg1对缺氧诱导的肺动脉和人肺动脉内皮细胞（HPAECs）的保护作用。结论：Rg1通过TXNIP/NLRP3通路调节氧化应激、炎症和线粒体自噬，改善缺氧诱导的肺血管内皮功能障碍。

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引用次数: 0

Non-saponin from Panax ginseng maintains blood-brain barrier integrity by inhibiting NF-κB and p38 MAP kinase signaling pathways to prevent the progression of experimental autoimmune encephalomyelitis 人参非皂苷通过抑制NF-κB和p38 MAP激酶信号通路维持血脑屏障完整性，防止实验性自身免疫性脑脊髓炎的进展。

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2025-01-01 DOI: 10.1016/j.jgr.2024.09.005

Jinhee Oh , Yujeong Ha , Tae Woo Kwon , Hyo-Sung Jo , Sang-Kwan Moon , Yoonsung Lee , Seung-Yeol Nah , Min Soo Kim , Ik-Hyun Cho

Background

The non-saponin (NS) fraction is an important active component of Panax ginseng, with multifunctional pharmacological activities including neuroprotective, immune regulatory, anti-inflammatory, and antioxidant effects. However, the effects of NSs on multiple sclerosis (MS), a chronic and autoimmune demyelinating disorder, have not yet been demonstrated.

Purpose

and Methods: The goal of the present study was to demonstrate the pharmacological actions of NSs on movement dysfunctions and the related mechanisms of action using an experimental autoimmune encephalomyelitis (EAE) mouse model of MS.

Results

NSs (p.o.) alleviated movement dysfunctions in EAE mice related to reduced demyelination in the lumbar spinal cord (LSC). NSs attenuated the recruitment of microglia (CD11b⁺/CD45^low) and macrophages (CD11b⁺/CD45^high) in LSCs from EAE model mice, consistent with the decreased mRNA expression levels of the main proinflammatory mediators (IL-1β, COX-2, MCP-1, MIP-1α, and RANTES). NSs blocked the migration of Th17 cells (CD4⁺/IL17A⁺) and mRNA expression levels of IL-17A (product of Th17 cells) in LSCs from EAE mice. NSs suppressed alterations in blood-brain barrier (BBB) components, such as astrocytes and cell adhesion molecules, associated with inhibiting NF-κB and p38 MAPK pathways in LSCs of EAE mice and lipopolysaccharide-induced bEND.3 cells.

Conclusions

NSs could attenuate movement dysfunctions and related pathological/inflammatory changes by reducing BBB permeability through NF-κB and p38 MAPK pathway inhibition in LSCs of EAE model mice. These are the first results suggesting that NSs can be potential therapeutic agents for MS by reducing BBB permeability.

背景：非皂苷（non-saponin， NS）部分是人参的重要活性成分，具有神经保护、免疫调节、抗炎、抗氧化等多种药理活性。然而，NSs对多发性硬化症（MS）（一种慢性自身免疫性脱髓鞘疾病）的影响尚未得到证实。目的和方法：本研究的目的是通过实验性自身免疫性脑脊髓炎（EAE）小鼠模型来证明NSs对运动功能障碍的药理作用及其相关的作用机制。结果：NSs （p.o o）减轻了与腰椎脱髓鞘（LSC）减少有关的EAE小鼠的运动功能障碍。NSs降低了EAE模型小鼠LSCs中小胶质细胞（CD11b+/CD45low）和巨噬细胞（CD11b+/CD45high）的募集，与主要促炎介质（IL-1β、COX-2、MCP-1、MIP-1α和RANTES） mRNA表达水平降低一致。NSs阻断了EAE小鼠LSCs中Th17细胞（CD4+/IL17A+）的迁移和Th17细胞产物IL-17A的mRNA表达水平。NSs抑制了血脑屏障（BBB）成分的改变，如星形胶质细胞和细胞粘附分子，这些成分与EAE小鼠LSCs中NF-κB和p38 MAPK通路的抑制以及脂多糖诱导的bEND有关。3细胞。结论：NSs可通过抑制EAE模型小鼠LSCs中NF-κB和p38 MAPK通路，降低血脑屏障通透性，减轻运动功能障碍及相关病理/炎症变化。这些结果首次表明NSs可以通过降低血脑屏障的通透性而成为MS的潜在治疗剂。

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引用次数: 0

Korean Red Ginseng-induced astrocytic HIF-1α: A key regulator of neuroglobin derived from neural stem cell differentiation in physiologic retina and brain 红参诱导的星形细胞HIF-1α：生理性视网膜和脑神经干细胞分化神经红蛋白的关键调节因子

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-31 DOI: 10.1016/j.jgr.2024.12.008

Sunhong Moon , Jinseo Park , Sueun Kim , Minsu Kim , Hui Su Jeon , Hyungsu Kim , Young-Myeong Kim , Ji-Yoon Kim , Yoon Kyung Choi

Background

Neuroglobin (Ngb) and growth-associated protein (GAP) 43 in neurons are associated with axonal regeneration. Korean Red Ginseng Extract (KRGE) enhances glial fibrillary acidic protein (GFAP)-positive astrocytes and hypoxia-inducible factor-1α (HIF-1α) protein activation in normoxic astrocytes. However, crosstalk between neural stem cell (NSC) differentiation and astrocytic HIF-1α in the KRGE-treated normoxic brain and retina remains unclear. We investigated whether KRGE-treated astrocytic HIF-1α can enhance NSC differentiation and increase the mature neurons expressing Ngb and GAP43.

Methods

Mature neuronal markers such as neuronal nuclei (NeuN) or microtubule-associated protein 2 (MAP2) were tested with Ngb in the mouse brain or retinal tissues post-KRGE administration. Direct KRGE treatment of NSCs or astrocytes was evaluated for Ngb levels. The KRGE-treated astrocyte conditioned media (ACM) were transferred to NSCs and HIF-1α levels were reduced using small interfering RNA transfection (si-HIF-1α) in astrocytes. si-HIF-1α-ACM with KRGE was tested for NSC differentiation.

Results

KRGE-administered mice showed significantly enhanced co-expression of Ngb with NeuN in the brain and MAP2 in the retina, along with the NSC marker Nestin, than water-administered mice. The KRGE treatment did not increase Ngb levels in NSCs, but stimulated astrocytes to secrete factors affecting NSCs’ differentiate into mature neurons and astrocytes. The KRGE-treated mouse retinas showed GFAP- and HIF-1α double-positive cells. Co-treatment with si-HIF-1α-transfected KRGE–ACM blocked KRGE–ACM-induced NSC differentiation into astrocytes or Ngb-expressing neurons.

Conclusion

KRGE stimulates astrocytic HIF-1α, which regulates NSC differentiation into mature neurons expressing Ngb, thereby promoting regeneration by enhancing NSC–astrocyte crosstalk in the physiological retina and brain.

神经元中的神经球蛋白（Ngb）和生长相关蛋白（GAP） 43与轴突再生有关。高丽红参提取物（KRGE）增强胶质纤维酸性蛋白（GFAP）阳性星形胶质细胞和缺氧诱导因子-1α (HIF-1α)蛋白的活性。然而，krge处理的正常大脑和视网膜中，神经干细胞（NSC）分化和星形细胞HIF-1α之间的串扰尚不清楚。我们研究了krge处理的星形细胞HIF-1α是否能促进NSC分化，增加Ngb和GAP43的成熟神经元表达。方法用Ngb检测krge给药后小鼠脑或视网膜组织中神经元核（NeuN）或微管相关蛋白2 （MAP2）等成熟神经元标志物。评价KRGE直接治疗NSCs或星形胶质细胞的Ngb水平。将krge处理的星形胶质细胞条件培养基（ACM）转移到NSCs中，通过小干扰RNA转染（si-HIF-1α）降低星形胶质细胞中的HIF-1α水平。si-HIF-1α-ACM结合KRGE进行NSC分化试验。结果与水给药小鼠相比，skrge给药小鼠脑内Ngb与NeuN、视网膜内MAP2及NSC标记物Nestin的共表达显著增强。KRGE处理并未增加Ngb水平，但刺激星形胶质细胞分泌影响NSCs向成熟神经元和星形胶质细胞分化的因子。krge处理的小鼠视网膜显示GFAP-和HIF-1α双阳性细胞。与si- hif -1α-转染的KRGE-ACM共处理可阻断KRGE-ACM诱导的NSC向星形胶质细胞或表达ngb的神经元的分化。结论krge刺激星形胶质细胞HIF-1α，调节NSC向表达Ngb的成熟神经元分化，从而通过增强生理视网膜和脑内NSC -星形胶质细胞串音促进再生。

{"title":"Korean Red Ginseng-induced astrocytic HIF-1α: A key regulator of neuroglobin derived from neural stem cell differentiation in physiologic retina and brain","authors":"Sunhong Moon , Jinseo Park , Sueun Kim , Minsu Kim , Hui Su Jeon , Hyungsu Kim , Young-Myeong Kim , Ji-Yoon Kim , Yoon Kyung Choi","doi":"10.1016/j.jgr.2024.12.008","DOIUrl":"10.1016/j.jgr.2024.12.008","url":null,"abstract":"<div><h3>Background</h3><div>Neuroglobin (Ngb) and growth-associated protein (GAP) 43 in neurons are associated with axonal regeneration. Korean Red Ginseng Extract (KRGE) enhances glial fibrillary acidic protein (GFAP)-positive astrocytes and hypoxia-inducible factor-1α (HIF-1α) protein activation in normoxic astrocytes. However, crosstalk between neural stem cell (NSC) differentiation and astrocytic HIF-1α in the KRGE-treated normoxic brain and retina remains unclear. We investigated whether KRGE-treated astrocytic HIF-1α can enhance NSC differentiation and increase the mature neurons expressing Ngb and GAP43.</div></div><div><h3>Methods</h3><div>Mature neuronal markers such as neuronal nuclei (NeuN) or microtubule-associated protein 2 (MAP2) were tested with Ngb in the mouse brain or retinal tissues post-KRGE administration. Direct KRGE treatment of NSCs or astrocytes was evaluated for Ngb levels. The KRGE-treated astrocyte conditioned media (ACM) were transferred to NSCs and HIF-1α levels were reduced using small interfering RNA transfection (si-HIF-1α) in astrocytes. si-HIF-1α-ACM with KRGE was tested for NSC differentiation.</div></div><div><h3>Results</h3><div>KRGE-administered mice showed significantly enhanced co-expression of Ngb with NeuN in the brain and MAP2 in the retina, along with the NSC marker Nestin, than water-administered mice. The KRGE treatment did not increase Ngb levels in NSCs, but stimulated astrocytes to secrete factors affecting NSCs’ differentiate into mature neurons and astrocytes. The KRGE-treated mouse retinas showed GFAP- and HIF-1α double-positive cells. Co-treatment with si-HIF-1α-transfected KRGE–ACM blocked KRGE–ACM-induced NSC differentiation into astrocytes or Ngb-expressing neurons.</div></div><div><h3>Conclusion</h3><div>KRGE stimulates astrocytic HIF-1α, which regulates NSC differentiation into mature neurons expressing Ngb, thereby promoting regeneration by enhancing NSC–astrocyte crosstalk in the physiological retina and brain.</div></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":"49 2","pages":"Pages 189-196"},"PeriodicalIF":6.8,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445814","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}

引用次数: 0

Corrigendum to ‘Reciprocal regulation of SIRT1 and AMPK by Ginsenoside compound K impedes the conversion from plasma cells to mitigate for podocyte injury in MRL/lpr mice in a B cell-specific manner’ [J Ginseng Res Volume 48 (2024) 190–201/JGR-D-23-00097] “人参皂苷化合物K对SIRT1和AMPK的相互调节阻碍了MRL/lpr小鼠的浆细胞转化，以B细胞特异性的方式减轻足细胞损伤”的更正[J人参研究vol 48 (2024) 190-201 /JGR-D-23-00097]

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-21 DOI: 10.1016/j.jgr.2024.12.006

Ziyu Song , Meng Jin , Shenglong Wang , Yanzuo Wu , Qi Huang , Wangda Xu , Yongsheng Fan , Fengyuan Tian

引用次数: 0

A narrative review of Panax notoginseng: Unique saponins and their pharmacological activities 三七的叙述综述：独特的皂苷及其药理活性

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-20 DOI: 10.1016/j.jgr.2024.12.005

Wenbiao Li, Hailian Shi, Xiaojun Wu

Panax notoginseng (PN) is a precious traditional Chinese medicine (TCM) whose medicinal parts are roots and rhizomes for the treatment of haemorrhage, blood-stasis, swelling and pain. It contains various compounds with saponins being the main active components for its therapeutic effects. A thorough analysis of the unique saponins present in aboveground and underground parts was performed by literature search and database screening. Compared with PN, other Panax genus like P. ginseng (PG), P. quinquefolium (PQ) and P. japonicus (PJ) have the similar chemical composition and pharmacologic effects but different applications based on the TCM theory. PG is renowned for its qi-tonifying properties, while PQ is known for its heat-clearing and fluid-nourishing effects. PJ can eliminate phlegm and relieve cough except for its stasis-dispelling and hemostatic properties like PN. PN, PG, and PQ feature damarane-type saponins, while PJ has a high content of oleic acid-type saponins. In this review, the saponins within the four species were classified and compared, and the unique saponins in PN were identified, such as notoginsenosides Ft1, B, Ab1-3, Fh1-9, etc., which may contribute to its special activities. And their pharmacological effects were also analyzed and summarized, suggesting that notoginsenoside Ft1 may be crucial for vascular homeostasis. However, the effect of unique saponins in PN on blood health should be well-clarified. This review highlights the importance of unique saponins in PN for its overall efficacy and hopes to make further exploration of their potential applications.

三七（Panax notoginseng， PN）是一种珍贵的中药，其药用部位是根和根茎，用于治疗出血、瘀血、肿胀和疼痛。它含有多种化合物，以皂苷为主要有效成分，具有治疗作用。通过文献检索和数据库筛选，对地上部分和地下部分的独特皂苷进行了深入的分析。人参（PG）、西洋参（PQ）和日本参（PJ）等其他人参属植物的化学成分和药理作用相似，但在中医理论基础上的应用不同。PG以其补气特性而闻名，而PQ则以其清热滋补功效而闻名。PJ除与PN具有化瘀止血作用外，还具有化痰止咳的作用。PN、PG、PQ以达玛烷型皂苷为主，PJ以油酸型皂苷含量较高。本文对这四种植物的皂苷进行了分类和比较，鉴定出了三七皂苷Ft1、B、Ab1-3、Fh1-9等可能与三七皂苷具有特殊活性有关的独特皂苷。并对其药理作用进行了分析和总结，提示三七皂苷Ft1可能对血管稳态起重要作用。然而，PN中独特的皂苷对血液健康的影响应该得到很好的澄清。本文综述了独特皂苷在PN中整体功效的重要性，并希望进一步探索其潜在的应用前景。

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引用次数: 0

Antiviral potential of ginseng: Targeting human pathogenic viruses with compounds derived from ginseng 人参的抗病毒潜力：用人参提取的化合物靶向人类病原病毒

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-10 DOI: 10.1016/j.jgr.2024.12.004

Chen Huo , Jihye Baek , Ki Hyun Kim

The COVID-19 pandemic has highlighted the critical need for effective antiviral therapies, as viral infections remain a leading cause of mortality worldwide. Natural compounds, especially those derived from plants, have been recognized for their therapeutic properties. Ginseng, in particular, has attracted considerable attention for its potential antiviral effects. This review examines the antiviral compounds from ginseng that act against various human pathogenic viruses. We systematically summarize the antiviral activities of ginseng compounds targeting a range of viruses, including human rhinovirus (HRV), influenza virus, human immunodeficiency virus (HIV), hepatitis viruses A, B, and C (HAV, HBV, HCV), herpes simplex virus (HSV), enterovirus 71 (EV71), coxsackievirus, norovirus, and SARS-CoV-2, the virus responsible for COVID-19. This review covers Panax ginseng, P. notoginseng, and P. quinquefolius, discussing their mechanisms of action and therapeutic potential. The analysis incorporates literature from February 2002 through August 2024, providing a comprehensive overview of the existing evidence on the antiviral properties of compounds derived from ginseng. This review aims to underscore the scientific basis for developing ginseng as an antiviral therapeutic agent or nutraceutical.

COVID-19大流行凸显了对有效抗病毒治疗的迫切需要，因为病毒感染仍然是全球死亡的主要原因。天然化合物，特别是从植物中提取的化合物，已被公认具有治疗作用。特别是人参，因其潜在的抗病毒作用而引起了相当大的关注。本文综述了人参中抗多种人类病原病毒的抗病毒化合物。我们系统地总结了人参化合物对一系列病毒的抗病毒活性，包括人类鼻病毒（HRV）、流感病毒、人类免疫缺陷病毒（HIV）、肝炎病毒a、B和C （HAV、HBV、HCV）、单纯疱疹病毒（HSV）、肠病毒71 （EV71）、柯萨奇病毒、诺如病毒和导致COVID-19的SARS-CoV-2。本文综述了人参、三七和西洋参的作用机制和治疗潜力。该分析纳入了2002年2月至2024年8月的文献，全面概述了人参中提取的化合物的抗病毒特性的现有证据。本文综述了人参作为抗病毒药物或营养品开发的科学依据。

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引用次数: 0

Anti-fatigue effects of Korean Red Ginseng extract in healthy Japanese adults: A randomized, double-blind, placebo-controlled study 红参提取物对健康日本成年人的抗疲劳作用：一项随机、双盲、安慰剂对照研究

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-06 DOI: 10.1016/j.jgr.2024.12.003

Yeong-Geun Lee , Woojae Hong , Young Mi Cho , Jeong Eun Kwon , Deok-Chun Yang , Hyunggun Kim , Se Chan Kang

Background

Chronic fatigue deleteriously affects the quality of life, thereby impairing physical and social functions and subsequently leading to financial and social problems. This study investigated the anti-fatigue effects of Korean Red Ginseng (KRG) extract in healthy middle-aged Japanese adults.

Methods

Forty-six participants were randomly divided into two groups (KRG and placebo). KRG (960 mg) or placebo capsules were administered for 3 weeks. The effect of KRG on fatigue was evaluated using visual analogue scale (VAS), plasma lactic acid, and cortisol levels.

Results and conclusions

Three-week consumption of KRG extract resulted in a significant decrease in the fatigue VAS score compared to the placebo group (p = 0.035). No significant difference was found in plasma cortisol and lactic acid levels between the groups. There were no differences between groups in the incidence of adverse events and the results of urinalysis, hematology, and biochemistry. These findings suggest the potential of KRG extract in mitigating fatigue and the safety of KRG extracts in healthy adults.

慢性疲劳有害地影响生活质量，从而损害身体和社会功能，并随后导致经济和社会问题。本研究探讨了红参提取物对日本健康中年成人的抗疲劳作用。方法46例患者随机分为KRG组和安慰剂组。KRG（960毫克）或安慰剂胶囊给予3周。采用视觉模拟量表（VAS）、血浆乳酸和皮质醇水平评估KRG对疲劳的影响。结果与结论与安慰剂组相比，服用三周KRG提取物可显著降低疲劳VAS评分（p = 0.035）。血浆皮质醇和乳酸水平在两组间无显著差异。两组间不良事件发生率及尿分析、血液学、生化结果均无差异。这些发现提示了KRG提取物在健康成人中缓解疲劳的潜力和KRG提取物的安全性。

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引用次数: 0

Ginsenoside Rg1 exerts antidepressant effect by regulating hepatic kynurenine metabolism through promoting the interaction between HNF4α and PGC1α 人参皂苷Rg1通过促进HNF4α和PGC1α的相互作用，调节肝脏犬尿氨酸代谢，发挥抗抑郁作用

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-12-04 DOI: 10.1016/j.jgr.2024.12.002

Keke Jia , Shuman Pan , Wenyuan Wu , Yiming Sun , Qingyu Zhang

Background

The neuroprotective effect of ginsenoside Rg1 is indeed one of the current research hotspots. However, its limited ability to cross the blood-brain barrier results in low distribution within the brain. Thus, the mechanism through which ginsenoside Rg1 affects the central nervous system needs further examination.

Methods

The LC-MS/MS analysis was used to detect the Kyn level. The expression of kynurenine aminotransferase 2 (KAT2) and kynurenine 3-monooxygenase (KMO) were investigated by qRT-PCR and western blotting analysis. The interaction between the transcription factor hepatocyte nuclear factor-4α (HNF4α) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) was explored by Co-IP assay. The HNF4α binding sites in the KAT2 and KMO genes were analyzed by ChIP. In addition, we specifically knocked down HNF4α in the liver of mice by injecting adeno-associated virus into the tail vein.

Results

Ginsenoside Rg1 upregulated the expression of KAT2 and KMO, thereby increasing the metabolism of Kyn in the liver. Further exploring its mechanism, we discovered that ginsenoside Rg1 increased the expression of KAT2 and KMO by promoting the interaction between the transcription factor HNF4α and PGC1α. Hepatic HNF4α knockdown abolished the antidepressant effects induced by ginsenoside Rg1.

Conclusion

Our findings reveal a novel mechanism in which ginsenoside Rg1 upregulates KAT2 and KMO through the HNF4α/PGC1α pathway, reducing hepatic Kyn levels and subsequently alleviating depression.

人参皂苷Rg1的神经保护作用确实是当前研究的热点之一。然而，它穿过血脑屏障的能力有限，导致其在大脑内的分布很低。因此，人参皂苷Rg1影响中枢神经系统的机制有待进一步研究。方法采用LC-MS/MS法检测Kyn含量。采用qRT-PCR和western blotting检测犬尿氨酸转氨酶2 （KAT2）和犬尿氨酸3-单加氧酶（KMO）的表达。采用Co-IP法探讨转录因子肝细胞核因子-4α (HNF4α)与过氧化物酶体增殖物激活受体-γ共激活因子-1α (PGC1α)之间的相互作用。用ChIP分析KAT2和KMO基因中的HNF4α结合位点。此外，我们通过向小鼠尾静脉注射腺相关病毒特异性地敲除了小鼠肝脏中的HNF4α。结果人参皂苷Rg1上调KAT2和KMO的表达，从而增加肝脏中Kyn的代谢。进一步探索其作用机制，我们发现人参皂苷Rg1通过促进转录因子HNF4α和PGC1α的相互作用而增加KAT2和KMO的表达。肝脏HNF4α敲低可消除人参皂苷Rg1诱导的抗抑郁作用。结论人参皂苷Rg1通过HNF4α/PGC1α通路上调KAT2和KMO，从而降低肝脏Kyn水平，从而缓解抑郁的新机制。

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引用次数: 0

Rare ginsenosides transformed from stems and leaves of Panax ginseng reverse obesity by promoting browning of white fat through PKA/CREB pathway via REGγ negative regulation 人参茎叶转化的稀有人参皂苷通过REGγ负调控PKA/CREB通路促进白色脂肪褐化，从而逆转肥胖

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research

Pub Date : 2024-11-28 DOI: 10.1016/j.jgr.2024.11.005

Jianbo Chen, Jiyue Sha, Xiaohui Huo, Zhiman Li, Di Qu, Xueqing Li, Meijia Li

Background

White adipose tissue (WAT) browning can promote thermogenesis and could be a promising target for treating obesity. Rare ginsenosides transformed from stems and leaves of Panax ginseng (T-GSSL) exhibit numerous biological activities. However, its potential anti-obesity effects and underlying mechanism remain largely unknown.

Methods

Five amino acids were selected as the catalysts for the transformation of ginsenosides into rare ginsenosides. An obese mouse model was established by feeding mice a high-fat diet (HFD) for 14 weeks. The effects of T-GSSL on obese mice were assessed by measuring body weight, fat mass, energy expenditure (EE), and glucose tolerance. The 3T3-L1 cells were differentiated into mature adipocytes and incubated with T-GSSL. Immunohistochemistry, co-immunoprecipitation (Co-IP), enzyme-linked immunosorbent assays (ELISA), western blotting (WB), real-time polymerase chain reaction (PCR), and other methods were used to investigate the targets and mechanisms of action of T-GSSL.

Results

Ginsenosides in GSSL were hydrolyzed using glutamic acid as a catalyst and 12 rare ginsenosides were produced, with a total conversion rate of 95 %. T-GSSL ameliorated metabolic disorders, lipid ectopic deposition, and obesity, and maintained glucose homeostasis in obese mice. T-GSSL treatment promoted adipose browning and enhanced EE in both HFD mice and 3T3-L1 cells. These effects were decreased in cells treated with a protein kinase A (PKA) antagonist or subjected to PKAcα knockdown, whereas they were increased in REGγ^−/− mice. The inhibition of REGγ alongside the activation of the PKA/CREB pathway elucidates the mechanism through which T-GSSL reverses obesity by promoting the browning of adipose tissue.

Conclusions

T-GSSL attenuates diet-induced obesity by promoting adipose browning through the inhibition of REGγ and subsequent activation of the PKA/CREB pathway.

白色脂肪组织（WAT）褐变可以促进产热，可能是治疗肥胖的一个有希望的靶点。从人参茎叶转化而来的稀有人参皂苷（T-GSSL）具有多种生物活性。然而，其潜在的抗肥胖作用和潜在的机制在很大程度上仍然未知。方法选择5种氨基酸作为催化人参皂苷转化为稀有人参皂苷的催化剂。采用高脂饲料（HFD）饲养14周，建立肥胖小鼠模型。通过测量体重、脂肪量、能量消耗（EE）和葡萄糖耐量来评估T-GSSL对肥胖小鼠的影响。将3T3-L1细胞分化为成熟脂肪细胞，用T-GSSL孵育。采用免疫组织化学、共免疫沉淀法（Co-IP）、酶联免疫吸附法（ELISA）、免疫印迹法（WB）、实时聚合酶链反应（PCR）等方法研究T-GSSL的作用靶点和作用机制。结果以谷氨酸为催化剂水解人参皂苷，制得12种稀有人参皂苷，总转化率达95%。T-GSSL改善了肥胖小鼠的代谢紊乱、脂质异位沉积和肥胖，并维持了葡萄糖稳态。T-GSSL处理促进HFD小鼠和3T3-L1细胞的脂肪褐变和EE增强。在蛋白激酶a （PKA）拮抗剂处理或PKAcα敲低的细胞中，这些作用减弱，而在REGγ−/−小鼠中则增加。REGγ的抑制和PKA/CREB通路的激活阐明了T-GSSL通过促进脂肪组织褐变逆转肥胖的机制。结论st - gssl通过抑制REGγ和随后激活PKA/CREB通路来促进脂肪褐变，从而减轻饮食诱导的肥胖。

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