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Qingxia Huang,Song Gao,Daqing Zhao,Xiangyan Li 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.3
Mitochondrial dysfunction contributes to the pathogenesis and prognosis of many common disorders, including neurodegeneration, stroke, myocardial infarction, tumor, and metabolic diseases. Ginsenosides, the major bioactive constituents of Panax ginseng (P. ginseng), have been reported to play beneficial roles in the molecular pathophysiology of these diseases by targeting mitochondrial dysfunction. In this review, we first introduce the types of ginsenosides and basic mitochondrial functions. Then, recent findings are summarized on different ginsenosides targeting mitochondria and their key signaling pathways for the treatment of multiple diseases, including neurological disorders, cancer, heart disease, hyperglycemia, and inflammation are summarized. This review may explain the common targets of ginsenosides against multiple diseases and provide new insights into the underlying mechanisms, facilitating research on the clinical application of P. ginseng.
Chen, Xuenan,Wang, Manying,Xu, Xiaohao,Liu, Jianzeng,Mei, Bing,Fu, Pingping,Zhao, Daqing,Sun, Liwei The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.3
Background: Recently, protein from ginseng was studied and used for the treatment of several kinds of diseases. However, the effect of ginseng total protein (GTP) on proliferation and wound healing in fibroblast cells remains unclear. Methods: In this study, cell viability was analyzed using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Cell cycle distribution was analyzed by flow cytometer. The levels of transforming growth factor ${\beta}1$, vascular endothelial growth factor, and collagens were analyzed by enzyme-linked immunosorbent assay and immunofluorescence staining. The expressions of cyclin A, phosphorylation of extracellular signal-related kinase (p-ERK1/2), and ERK1/2 were analyzed by Western blotting. Results: Our results showed that GTP promoted cell proliferation and increased the percentage of cells in S phase through the upregulation of cyclin A in NIH/3T3 cells. We also found that GTP induced the secretion of type I collagen, and promoted the expression of other factors that regulate the synthesis of collagen such as transforming growth factor ${\beta}1$ and vascular endothelial growth factor. In addition, the phosphorylation of ERK1/2 at Thr202/Tyr204 was also increased by GTP. Conclusion: Our studies suggest that GTP promoted proliferation and secretion of collagen in NIH/3T3 cells by activating the ERK signal pathway, which shed light on a potential function of GTP in promoting wound healing.
Jianzeng Liu,Xiaohao Xu,Jingyuan Zhou,Guang Sun,Zhenzhuo Li,Lu Zhai,Jing Wang,Rui Ma,Daqing Zhao,Rui Jiang,Liwei Sun 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Our previous investigation indicated that the preparation of Panax ginseng Meyer(P. ginseng) inhibited melanogenesis. It comprised salicylic acid (SA), protocatechuic acid (PA), p-coumaricacid (p-CA), vanillic acid (VA), and caffeic acid (CA). In this investigation, the regulatory effects ofP. ginseng phenolic acid monomers on melanin production were assessed. Methods: In vitro and in vivo impact of phenolic acid monomers were assessed. Results: SA, PA, p-CA and VA inhibited tyrosinase (TYR) to reduce melanin production, whereas CA hadthe opposite effects. SA, PA, p-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 ofTYR, 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 proteinlevel in a-MSH-stimulated B16F10 cells, comparable to untreated B16F10, increasing the expression ofphosphorylation glycogen synthase kinase 3b (p-GSK3b), b-catenin, p-ERK/ERK, and p-p38/p38. Furthermore, the GSK3b inhibitor promoted p-GSK3b and p-MITF expression, as observed in CA-treatedcells. Moreover, p38 and ERK inhibitors inhibited CA-stimulated p-p38/p38, p-ERK/ERK, and p-MITFincrease, which had negative binding energies with MC1R, as depicted by molecular docking. Conclusion: P. ginseng roots' phenolic acid monomers can safely inhibit melanin production by bidirectionallyregulating melanin synthase transcription. Furthermore, they reduced MITF expression viaMC1R/cAMP/PKA signaling pathway and enhanced MITF post-translational modification via Wnt/mitogen-activated protein kinase signaling pathway.
Ginsenosides repair UVB-induced skin barrier damage in BALB/c hairless mice and HaCaT keratinocytes
Zhenzhuo Li,Rui Jiang,Manying Wang,Lu Zhai,Jianzeng Liu,Xiaohao Xu,Liwei Sun,Daqing Zhao 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1
Background: Ginsenosides (GS) have potential value as cosmetic additives for prevention of skin photoaging. However, their protective mechanisms against skin barrier damage and their active monomeric constituents are unknown. Methods: GS monomer types and their relative proportions were identified. A UVB-irradiated BALB/c hairless mouse model was used to assess protective effects of GS components on skin epidermal thickness and transepidermal water loss (TEWL). Skin barrier function, reflected by filaggrin (FLG), involucrin (IVL), claudin-1 (Cldn-1), and aquaporin 3 (AQP3) levels and MAPK phosphorylation patterns, were analyzed in UVB-irradiated hairless mice or HaCaT cells. Results: Total GS monomeric content detected by UPLC was 85.45% and was largely attributed to 17 main monomers that included Re (16.73%), Rd (13.36%), and Rg1 (13.38%). In hairless mice, GS ameliorated UVB-induced epidermal barrier dysfunction manifesting as increased epidermal thickness, increased TEWL, and decreased stratum corneum water content without weight change. Furthermore, GS treatment of UVB-irradiated mice restored protein expression levels and epidermal tissue distributions of FLG, IVL, Cldn-1, and AQP3, with consistent mRNA and protein expression results obtained in UVB-irradiated HaCaT cells (except for unchanging Cldn-1 expression). Mechanistically, GS inhibited JNK, p38, and ERK phosphorylation in UVB-irradiated HaCaT cells, with a mixture of Rg2, Rg3, Rk3, F2, Rd, and Rb3 providing the same protective MAPK pathway inhibition-associated upregulation of IVL and AQP3 expression as provided by intact GS treatment. Conclusion: GS protection against UVB-irradiated skin barrier damage depends on activities of six ginsenoside monomeric constituents that inhibit the MAPK signaling pathway.
Qingxia Huang,Jing Li,Jinjin Chen,Zepeng Zhang,Peng Xu,Hongyu Qi,Zhaoqiang Chen,Jiaqi Liu,Jing Lu,Mengqi Shi,Yibin Zhang,Ying Ma,Daqing Zhao,Xiangyan Li The Korean Society of Ginseng 2023 Journal of Ginseng Research Vol.47 No.3
Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.
Huang, Qingxia,Lou, Tingting,Lu, Jing,Wang, Manying,Chen, Xuenan,Xue, Linyuan,Tang, Xiaolei,Qi, Wenxiu,Zhang, Zepeng,Su, Hang,Jin, Wenqi,Jing, Chenxu,Zhao, Daqing,Sun, Liwei,Li, Xiangyan The Korean Society of Ginseng 2022 Journal of Ginseng Research Vol.46 No.6
Background: Aerobic cellular respiration provides chemical energy, adenosine triphosphate (ATP), to maintain multiple cellular functions. Sirtuin 1 (SIRT1) can deacetylate peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) to promote mitochondrial biosynthesis. Targeting energy metabolism is a potential strategy for the prevention and treatment of various diseases, such as cardiac and neurological disorders. Ginsenosides, one of the major bioactive constituents of Panax ginseng, have been extensively used due to their diverse beneficial effects on healthy subjects and patients with different diseases. However, the underlying molecular mechanisms of total ginsenosides (GS) on energy metabolism remain unclear. Methods: In this study, oxygen consumption rate, ATP production, mitochondrial biosynthesis, glucose metabolism, and SIRT1-PGC-1α pathways in untreated and GS-treated different cells, fly, and mouse models were investigated. Results: GS pretreatment enhanced mitochondrial respiration capacity and ATP production in aerobic respiration-dominated cardiomyocytes and neurons, and promoted tricarboxylic acid metabolism in cardiomyocytes. Moreover, GS clearly enhanced NAD<sup>+</sup>-dependent SIRT1 activation to increase mitochondrial biosynthesis in cardiomyocytes and neurons, which was completely abrogated by nicotinamide. Importantly, ginsenoside monomers, such as Rg1, Re, Rf, Rb1, Rc, Rh1, Rb2, and Rb3, were found to activate SIRT1 and promote energy metabolism. Conclusion: This study may provide new insights into the extensive application of ginseng for cardiac and neurological protection in healthy subjects and patients.