Journal of Ginseng Research最新文献

{"title":"Ginsenoside Rg5 promotes wound healing in diabetes by reducing the negative regulation of SLC7A11 on the efferocytosis of dendritic cells","authors":"Wei Xia ,&nbsp;Zongdong Zhu ,&nbsp;Song Xiang ,&nbsp;Yi Yang","doi":"10.1016/j.jgr.2023.06.006","DOIUrl":"10.1016/j.jgr.2023.06.006","url":null,"abstract":"<div><p>Background: ginsenoside Rg5 is a rare ginsenoside with known hypoglycemic effects in diabetic mice. This study aimed to explore the effects of ginsenoside Rg5 on skin wound-healing in the <em>Lepr</em>^{<em>db/db</em>} mutant (<em>db/db</em>) mice (C57BL/KsJ background) model and the underlying mechanisms.</p></div><div><h3>Methods</h3><p>Seven-week-old male C57BL/6J, <em>SLC7A11</em>-knockout (KO), the littermate wild-type (WT), and <em>db/db</em> mice were used for <em>in vivo</em> and <em>ex vivo</em> studies.</p></div><div><h3>Results</h3><p>Ginsenoside Rg5 provided through oral gavage in <em>db/db</em> mice significantly alleviated the abundance of apoptotic cells in the wound areas and facilitated skin wound healing. 50 μM ginsenoside Rg5 treatment nearly doubled the efferocytotic capability of bone marrow-derived dendritic cells (BMDCs) from <em>db/db</em> mice. It also reduced NF-κB p65 and <em>SLC7A11</em> expression in the wounded areas of <em>db/db</em> mice dose-dependently. Ginsenoside Rg5 physically interacted with SLC7A11 and suppressed the cystine uptake and glutamate secretion of BMDCs from <em>db/db</em> and <em>SLC7A1</em>1-WT mice but not in BMDCs from <em>SLC7A11-</em>KO mice. In BMDCs and conventional type 1 dendritic cells (cDC1s), ginsenoside Rg5 reduced their glycose storage and enhanced anaerobic glycolysis. Glycogen phosphorylase inhibitor CP-91149 almost abolished the effect of ginsenoside Rg5 on promoting efferocytosis. Conclusion: ginsenoside Rg5 can suppress the expression of SLC7A11 and inhibit its activity via physical binding. These effects collectively alleviate the negative regulations of SLC7A11 on anaerobic glycolysis, which fuels the efferocytosis of dendritic cells. Therefore, ginsenoside Rg5 has a potential adjuvant therapeutic reagent to support patients with wound-healing problems, such as diabetic foot ulcers.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000726/pdfft?md5=22b32861715ef40999b1d8b10c43661e&pid=1-s2.0-S1226845323000726-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42586187","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}

{"title":"Ginsenoside Rg5 promotes muscle regeneration via p38MAPK and Akt/mTOR signaling","authors":"Ryuni Kim ,&nbsp;Jee Won Kim ,&nbsp;Hyerim Choi ,&nbsp;Ji-Eun Oh ,&nbsp;Tae Hyun Kim ,&nbsp;Ga-Yeon Go ,&nbsp;Sang-Jin Lee ,&nbsp;Gyu-Un Bae","doi":"10.1016/j.jgr.2023.06.004","DOIUrl":"10.1016/j.jgr.2023.06.004","url":null,"abstract":"<div><h3>Background</h3><p>Skeletal muscles play a key role in physical activity and energy metabolism. The loss of skeletal muscle mass can cause problems related to metabolism and physical activity. Studies are being conducted to prevent such diseases by increasing the mass and regeneration capacity of muscles. Ginsenoside Rg5 has been reported to exhibit a broad range of pharmacological activities. However, studies on the effects of Rg5 on muscle differentiation and growth are scarce.</p></div><div><h3>Methods</h3><p>To investigate the effects of Rg5 on myogenesis, C2C12 myoblasts were induced to differentiate with Rg5, followed by immunoblotting, immunostaining, and qRT-PCR for myogenic markers and promyogenic signaling (p38MAPK). Immunoprecipitation confirmed that Rg5 increased the interaction between MyoD and E2A <em>via</em> p38MAPK. To investigate the effects of Rg5 on prevention of muscle mass loss, C2C12 myotubes were treated with dexamethasone to induce muscle atrophy. Immunoblotting, immunostaining, and qRT-PCR were performed for myogenic markers, Akt/mTOR signaling for protein synthesis, and atrophy-related genes (Atrogin-1 and MuRF1).</p></div><div><h3>Results</h3><p>Rg5 promoted C2C12 myoblast differentiation through phosphorylation of p38MAPK and MyoD/E2A heterodimerization. Furthermore, Rg5 stimulated C2C12 myotube hypertrophy <em>via</em> phosphorylation of Akt/mTOR. Phosphorylation of Akt induces FoxO3a phosphorylation, which reduces the expression of Atrogin-1 and MuRF1.</p></div><div><h3>Conclusion</h3><p>This study provides an understanding of how Rg5 promotes myogenesis and hypertrophy and prevents dexamethasone-induced muscle atrophy. The study is the first, to the best of our knowledge, to show that Rg5 promotes muscle regeneration and to suggest that Rg5 can be used for therapeutic intervention of muscle weakness and atrophy, including cancer cachexia.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000702/pdfft?md5=30085717af922d3493fa7dc43b2388fa&pid=1-s2.0-S1226845323000702-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43684553","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}

{"title":"Methods on improvements of the poor oral bioavailability of ginsenosides: Pre-processing, structural modification, drug combination, and micro- or nano- delivery system","authors":"Qi-rui Hu ,&nbsp;Huan Hong ,&nbsp;Zhi-hong Zhang ,&nbsp;Hua Feng ,&nbsp;Ting Luo ,&nbsp;Jing Li ,&nbsp;Ze-yuan Deng ,&nbsp;Fang Chen","doi":"10.1016/j.jgr.2023.07.005","DOIUrl":"10.1016/j.jgr.2023.07.005","url":null,"abstract":"<div><p>Panax ginseng Meyer is a traditional Chinese medicine that is widely used as tonic in Asia. The main pharmacologically active components of ginseng are the dammarane-type ginsenosides, which have been shown to have anti-cancer, anti-inflammatory, immunoregulatory, neuroprotective, and metabolic regulatory activities. Moreover, some of ginsenosides (eg, Rh2 and Rg3) have been developed into nutraceuticals. However, the utilization of ginsenosides in clinic is restrictive due to poor permeability in cells and low bioavailability in human body. Obviously, the dammarane skeleton and glycosyls of ginsenosides are responsible for these limitations. Therefore, improving the oral bioavailability of ginsenosides has become a pressing issue. Here, based on the structures of ginsenosides, we summarized the understanding of the factors affecting the oral bioavailability of ginsenosides, introduced the methods to enhance the oral bioavailability and proposed the future perspectives on improving the oral bioavailability of ginsenosides.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000799/pdfft?md5=5e3f00e336bd90bb9e2ed327e2b28ece&pid=1-s2.0-S1226845323000799-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41973593","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}

{"title":"Phenolic acids in Panax ginseng inhibit melanin production through bidirectional regulation of melanin synthase transcription via different signaling pathways","authors":"Jianzeng Liu ,&nbsp;Xiaohao Xu ,&nbsp;Jingyuan Zhou ,&nbsp;Guang Sun ,&nbsp;Zhenzhuo Li ,&nbsp;Lu Zhai ,&nbsp;Jing Wang ,&nbsp;Rui Ma ,&nbsp;Daqing Zhao ,&nbsp;Rui Jiang ,&nbsp;Liwei Sun","doi":"10.1016/j.jgr.2023.05.002","DOIUrl":"10.1016/j.jgr.2023.05.002","url":null,"abstract":"<div><h3>Background</h3><p>Our previous investigation indicated that the preparation of <em>Panax ginseng</em> Meyer (<em>P. ginseng</em>) inhibited melanogenesis. It comprised salicylic acid (SA), protocatechuic acid (PA), <em>p</em>-coumaric acid (<em>p</em>-CA), vanillic acid (VA), and caffeic acid (CA). In this investigation, the regulatory effects of <em>P. ginseng</em> phenolic acid monomers on melanin production were assessed.</p></div><div><h3>Methods</h3><p><em>In vitro and in vivo</em> impact of phenolic acid monomers were assessed.</p></div><div><h3>Results</h3><p>SA, PA, <em>p</em>-CA and VA inhibited tyrosinase (TYR) to reduce melanin production, whereas CA had the opposite effects. SA, PA, <em>p</em>-CA and VA significantly downregulated the melanocortin 1 receptor (MC1R), cycle AMP (cAMP), protein kinase A (PKA), cycle AMP-response element-binding protein (CREB), microphthalmia-associated transcription factor (MITF) pathway, reducing mRNA and protein levels of TYR, tyrosinase-related protein 1 (TYRP1), and TYRP2. Moreover, CA treatment enhanced the cAMP, PKA, and CREB pathways to promote MITF mRNA level and phosphorylation. It also alleviated MITF protein level in α-MSH-stimulated B16F10 cells, comparable to untreated B16F10, increasing the expression of phosphorylation glycogen synthase kinase 3β (p-GSK3β), β-catenin, p-ERK/ERK, and p-p38/p38. Furthermore, the GSK3β inhibitor promoted p-GSK3β and p-MITF expression, as observed in CA-treated cells. Moreover, p38 and ERK inhibitors inhibited CA-stimulated p-p38/p38, p-ERK/ERK, and p-MITF increase, which had negative binding energies with MC1R, as depicted by molecular docking.</p></div><div><h3>Conclusion</h3><p><em>P. ginseng</em> roots' phenolic acid monomers can safely inhibit melanin production by bidirectionally regulating melanin synthase transcription. Furthermore, they reduced MITF expression via MC1R/cAMP/PKA signaling pathway and enhanced MITF post-translational modification via Wnt/mitogen-activated protein kinase signaling pathway.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000556/pdfft?md5=01f972dfbf3be2134932adcbf890bfe0&pid=1-s2.0-S1226845323000556-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46461806","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}

{"title":"20(S)-ginsenoside Rg3 exerts anti-fibrotic effect after myocardial infarction by alleviation of fibroblasts proliferation and collagen deposition through TGFBR1 signaling pathways","authors":"Honglin Xu ,&nbsp;Haifeng Miao ,&nbsp;Guanghong Chen ,&nbsp;Guoyong Zhang ,&nbsp;Yue Hua ,&nbsp;Yuting Wu ,&nbsp;Tong Xu ,&nbsp;Xin Han ,&nbsp;Changlei Hu ,&nbsp;Mingjie Pang ,&nbsp;Leyi Tan ,&nbsp;Bin Liu ,&nbsp;Yingchun Zhou","doi":"10.1016/j.jgr.2023.06.007","DOIUrl":"10.1016/j.jgr.2023.06.007","url":null,"abstract":"<div><h3>Background</h3><p>Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiac remodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovascular diseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effect post-MI.</p></div><div><h3>Methods</h3><p>Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-β1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin and Masson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effects of Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 was explored by surface plasmon resonance imaging (SPRi). Moreover, myocardial <em>Tgfbr1</em>-deficient mice and TGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3.</p></div><div><h3>Results</h3><p><em>In vivo</em> experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiac function. Rg3-TGFBR1 had the 1.78 × 10⁻⁷ M equilibrium dissociation constant based on SPRi analysis, and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific <em>Tgfbr1</em> knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 down-regulated the TGF-β1-mediated CFs growth together with collagen production <em>in vitro</em> through TGFBR1 signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3.</p></div><div><h3>Conclusion</h3><p>Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferation along with collagen deposition by inactivation of TGFBR1 pathway.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000738/pdfft?md5=233d9e4efb492af19ea96fd3ad09020b&pid=1-s2.0-S1226845323000738-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42408251","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}

{"title":"Anti-thrombotic effects of ginsenoside Rk3 by regulating cAMP and PI3K/MAPK pathway on human platelets","authors":"Hyuk-Woo Kwon ,&nbsp;Jung-Hae Shin ,&nbsp;Man Hee Rhee ,&nbsp;Chang-Eun Park ,&nbsp;Dong-Ha Lee","doi":"10.1016/j.jgr.2023.04.006","DOIUrl":"10.1016/j.jgr.2023.04.006","url":null,"abstract":"<div><h3>Background and objective</h3><p>The ability to inhibit aggregation has been demonstrated with synthetically derived ginsenoside compounds G-Rp (1, 3, and 4) and ginsenosides naturally found in <em>Panax ginseng</em> 20(S)-Rg3, Rg6, F4, and Ro. Among these compounds, Rk3 (G-Rk3) from <em>Panax ginseng</em> needs to be further explored in order to reveal the mechanisms of action during inhibition.</p></div><div><h3>Methodology</h3><p>Our study focused to investigate the action of G-Rk3 on agonist-stimulated human platelet aggregation, inhibition of platelet signaling molecules such as fibrinogen binding with integrin α_IIbβ₃ using flow cytometry, intracellular calcium mobilization, dense granule secretion, and thromboxane B₂ secretion. In addition, we checked the regulation of phosphorylation on PI3K/MAPK pathway, and thrombin-induced clot retraction was also observed in platelets rich plasma.</p></div><div><h3>Key Results</h3><p>G-Rk3 significantly increased amounts of cyclic adenosine monophosphate (cAMP) and led to significant phosphorylation of cAMP-dependent kinase substrates vasodilator-stimulated phosphoprotein (VASP) and inositol 1,4,5-trisphosphate receptor (IP₃R). In the presence of G-Rk3, dense tubular system Ca²⁺ was inhibited, and platelet activity was lowered by inactivating the integrin αIIb/β₃ and reducing the binding of fibrinogen. Furthermore, the effect of G-Rk3 extended to the inhibition of MAPK and PI3K/Akt phosphorylation resulting in the reduced secretion of intracellular granules and reduced production of TXA₂. Lastly, G-Rk3 inhibited platelet aggregation and thrombus formation via fibrin clot.</p></div><div><h3>Conclusions and implications</h3><p>These results suggest that when dealing with cardiovascular diseases brought upon by faulty aggregation among platelets or through the formation of a thrombus, the G-Rk3 compound can play a role as an effective prophylactic or therapeutic agent.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323000350/pdfft?md5=9edb6bc10c6e4507a8b4726b83b72b48&pid=1-s2.0-S1226845323000350-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47613374","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}

{"title":"The effects of Korean Red Ginseng on stress-related neurotransmitters and gene expression: A randomized, double-blind, placebo-controlled trial","authors":"Jihyun Yoon ,&nbsp;Byoungjin Park ,&nbsp;Kyung-Won Hong ,&nbsp;Dong-Hyuk Jung","doi":"10.1016/j.jgr.2023.08.001","DOIUrl":"10.1016/j.jgr.2023.08.001","url":null,"abstract":"<div><h3>Background</h3><p>Korean Red Ginseng (KRG) is an effective anti-stress treatment. In this study, we investigated the therapeutic potential effects of KRG on relieving stress in a general population using transcriptome analysis.</p></div><div><h3>Methods</h3><p>We conducted an 8-week clinical pilot study on 90 healthy men who reported stress. The study was completed by 43 participants in the KRG group and 44 participants in the placebo group. Participants were randomized 1:1 to the KRG and placebo groups. We evaluated the stress by stress response inventory (SRI) at baseline and 8 weeks. The main outcomes were changes in the levels of neurotransmitters (NTs) and NT-related gene expression. NTs were analyzed using automated (GC) content, and levels of gene expression were measured by reads per kilobase of transcript per million mapped reads (RPKM).</p></div><div><h3>Results</h3><p>The KRG group showed significantly preserved epinephrine decrease compared with placebo group at 8 weeks (changes in epinephrine, KRG vs. placebo; −1623.2 ± 46101.5 vs. −35116.3 ± 86288.2, p = 0012). Among subjects who higher SRI score, meaning stress increased compared to baseline, the KRG group showed a smaller decrease in serotonin than the placebo group (changes in serotonin, KRG vs. placebo; −2627.5 ± 5859.1 vs, −8087.4 ± 7162.4, p = 0.005) and a smaller increase in cortisol than the placebo group (changes in cortisol, KRG vs. placebo; 1912.7 ± 10097.75 vs. 8046.2 ± 8050.6 , p = 0.019) in subgroup analysis. Transcriptome findings indicated that KRG intake affects gene expression related with metabolism of choline, adrenalin, and monoamine.</p></div><div><h3>Conclusion</h3><p>These findings suggest that KRG has beneficial effects on the amelioration of stress response in NTs, and this effect is more prominent in stressful situations. Further clinical studies are required to confirm the anti-stress effect of KRG.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1226845323001069/pdfft?md5=c4d3f89c8370c4bed6a7529c82f948da&pid=1-s2.0-S1226845323001069-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48579918","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}

{"title":"Korean Red Ginseng extract ameliorates demyelination by inhibiting infiltration and activation of immune cells in cuprizone-administrated mice","authors":"Min Jung Lee ,&nbsp;Jong Hee Choi ,&nbsp;Tae Woo Kwon ,&nbsp;Hyo-Sung Jo ,&nbsp;Yujeong Ha ,&nbsp;Seung-Yeol Nah ,&nbsp;Ik-Hyun Cho","doi":"10.1016/j.jgr.2023.05.001","DOIUrl":"10.1016/j.jgr.2023.05.001","url":null,"abstract":"<div><h3>Background</h3><p>Korean Red Ginseng (KRG), the steamed root of <em>Panax ginseng</em>, has pharmacological activities for immunological and neurodegenerative disorders. But, the role of KRGE in multiple sclerosis (MS) remains unclear.</p></div><div><h3>Purpose</h3><p>To determine whether KRG extract (KRGE) could inhibit demyelination in corpus callosum (CC) of cuprizone (CPZ)-induced murine model of MS</p></div><div><h3>Methods</h3><p>Male adult mice were fed with a standard chow diet or a chow diet supplemented with 0.2% (w/w) CPZ <em>ad libitum</em> for six weeks to induce demyelination while were simultaneously administered with distilled water (DW) alone or KRGE-DW (0.004%, 0.02 and 0.1% of KRGE) by drinking.</p></div><div><h3>Results</h3><p>Administration with KRGE-DW alleviated demyelination and oligodendrocyte degeneration associated with inhibition of infiltration and activation of resident microglia and monocyte-derived macrophages as well as downregulation of proinflammatory mediators in the CC of CPZ-fed mice. KRGE-DW also attenuated the level of infiltration of Th1 and Th17) cells, in line with inhibited mRNA expression of IFN-γ and IL-17, respectively, in the CC. These positive effects of KRGE-DW mitigated behavioral dysfunction based on elevated plus maze and the rotarod tests.</p></div><div><h3>Conclusion</h3><p>The results strongly suggest that KRGE-DW may inhibit CPZ-induced demyelination due to its oligodendroglial protective and anti-inflammatory activities by inhibiting infiltration/activation of immune cells. Thus, KRGE might have potential in therapeutic intervention for MS.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8a/de/main.PMC10499591.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10300436","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}

{"title":"Skin wound healing effects of (+)-syringaresinol from ginseng berry","authors":"Jee-hyun Hwang ,&nbsp;Yeonsoo Kang ,&nbsp;Heui-Jin Park ,&nbsp;Seolyeong Kim ,&nbsp;Su-Hyun Lee ,&nbsp;Hangun Kim ,&nbsp;Sang-Jip Nam ,&nbsp;Kyung-Min Lim","doi":"10.1016/j.jgr.2023.04.003","DOIUrl":"10.1016/j.jgr.2023.04.003","url":null,"abstract":"<div><h3>Background</h3><p>Ginseng has been used as a traditional medicine and functional cosmetic ingredients for many years. Recent studies have focused on the potential biological effects of the ginseng berry and its ingredients. (+)-Syringaresinol (SYR) is enriched in ginseng berry and its beneficial effects on the skin have been recently reported. However, little is known about the its effects on the wound healing process of skin.</p></div><div><h3>Methods</h3><p>Here, we evaluated the skin wound healing effect of (+)-SYR using the human fibroblast Hs68 cell and <em>ex vivo</em> pig and human skin tissue model. Scratch wound test and hydrogen peroxide (HPO) induce chemical wound model were employed.</p></div><div><h3>Results</h3><p>(+)-SYR promoted the migration and proliferation of Hs68 cells without significant cytotoxicity at the tested concentrations. Especially, in <em>ex vivo</em> pig and human skin tissue, HPO-induced chemical wound was recovered almost completely by (+)-SYR. In line with the finding in Hs68, the protein expression levels of TGF-β and PCNA, a proliferation marker were increased, demonstrating the beneficial effects of (+)-SYR on skin wound repair.</p></div><div><h3>Conclusion</h3><p>Collectively, we demonstrated that (+)-SYR from ginseng berry, can enhance the wound healing effect by accelerating cell proliferation and skin regeneration, suggesting the potential utility of (+)-SYR for skin wound repair.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/db/65/main.PMC10499580.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10672533","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}

{"title":"The effects of Korean Red Ginseng on heme oxygenase-1 with a focus on mitochondrial function in pathophysiologic conditions","authors":"Chang-Hee Kim ,&nbsp;Hahn Young Kim ,&nbsp;Seung-Yeol Nah ,&nbsp;Yoon Kyung Choi","doi":"10.1016/j.jgr.2023.04.001","DOIUrl":"10.1016/j.jgr.2023.04.001","url":null,"abstract":"<div><p>Korean Red Ginseng (KRG) plays a key role in heme oxygenase (HO)-1 induction under physical and moderate oxidative stress conditions. The transient and mild induction of HO-1 is beneficial for cell protection, mitochondrial function, regeneration, and intercellular communication. However, chronic HO-1 overexpression is detrimental in severely injured regions. Thus, in a chronic pathological state, diminishing HO-1-mediated ferroptosis is beneficial for a therapeutic approach. The molecular mechanisms by which KRG protects various cell types in the central nervous system have not yet been established, especially in terms of HO-1-mediated mitochondrial functions. Therefore, in this review, we discuss the multiple roles of KRG in the regulation of astrocytic HO-1 under pathophysiological conditions. More specifically, we discuss the role of the KRG-mediated astrocytic HO-1 pathway in regulating mitochondrial functions in acute and chronic neurodegenerative diseases as well as physiological conditions.</p></div>","PeriodicalId":16035,"journal":{"name":"Journal of Ginseng Research","volume":null,"pages":null},"PeriodicalIF":6.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/38/a1/main.PMC10499582.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10308465","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}