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  • Frontiers Media SA  (47)
  • 1
    Online Resource
    Online Resource
    Corrigendum: Ginsenoside Compound K Enhances Fracture Healing via Promoting Osteogenesis and Angiogenesis
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology ( 2022-6-16)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, ( 2022-6-16)
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2022.952598
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 2
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    Ginsenoside Compound K Enhances Fracture Healing via Promoting Osteogenesis and Angiogenesis
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-4-1)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-4-1)
    Abstract: Fractures have an extraordinarily negative impact on an individual’s quality of life and functional status, particularly delayed or non-union fractures. Osteogenesis and angiogenesis are closely related to bone growth and regeneration, and bone modeling and remodeling. Recently Chinese medicine has been extensively studied to promote osteogenic differentiation in MSCs. Studies have found that Ginseng can be used as an alternative for tissue regeneration and engineering. Ginseng is a commonly used herbal medicine in clinical practice, and one of its components, Ginsenoside Compound K (CK), has received much attention. Evidence indicates that CK has health-promoting effects in inflammation, atherosclerosis, diabetics, aging, etc. But relatively little is known about its effect on bone regeneration and the underlying cellular and molecular mechanisms. In this study, CK was found to promote osteogenic differentiation of rat bone marrow mesenchymal stem cells (rBMSCs) by RT-PCR and Alizarin Red S staining in vitro . Mechanistically, we found CK could promote osteogenesis through activating Wnt/β-catenin signaling pathway by immunofluorescence staining and luciferase reporter assay. And we also showed that the tube formation capacity of human umbilical vein endothelial cells (HUVECs) was increased by CK. Furthermore, using the rat open femoral fracture model, we found that CK could improve fracture repair as demonstrated by Micro-CT, biomechanical and histology staining analysis. The formation of H type vessel in the fracture callus was also increased by CK. These findings provide a scientific basis for treating fractures with CK, which may expand its application in clinical practice.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2022.855393
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 3
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    Data_Sheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Microbiology Vol. 13 ( 2022-4-19)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 13 ( 2022-4-19)
    Abstract: Gut microbiota plays an important role in metabolic homeostasis. Previous studies demonstrated that ginsenoside Rb1 might improve obesity-induced metabolic disorders through regulating glucose and lipid metabolism in the liver and adipose tissues. Due to low bioavailability and enrichment in the intestinal tract of Rb1, we hypothesized that modulation of the gut microbiota might account for its pharmacological effects as well. Here, we show that oral administration of Rb1 significantly decreased serum LDL-c, TG, insulin, and insulin resistance index (HOMA-IR) in mice with a high-fat diet (HFD). Dynamic profiling of the gut microbiota showed that this metabolic improvement was accompanied by restoring of relative abundance of some key bacterial genera. In addition, the free fatty acids profiles in feces were significantly different between the HFD-fed mice with or without Rb1. The content of eight long-chain fatty acids (LCFAs) was significantly increased in mice with Rb1, which was positively correlated with the increase of Akkermansia and Parasuttereller , and negatively correlated with the decrease of Oscillibacter and Intestinimonas . Among these eight increased LCFAs, eicosapentaenoic acid (EPA), octadecenoic acids, and myristic acid were positively correlated with metabolic improvement. Furthermore, the colonic expression of the free fatty acid receptors 4 ( Ffar4 ) gene was significantly upregulated after Rb1 treatment, in response to a notable increase of LCFA in feces. These findings suggested that Rb1 likely modulated the gut microbiota and intestinal free fatty acids profiles, which should be beneficial for the improvement of metabolic disorders in HFD-fed mice. This study provides a novel mechanism of Rb1 for the treatment of metabolic disorders induced by obesity, which may provide a therapeutic avenue for the development of new nutraceutical-based remedies for treating metabolic diseases, such as hyperlipidemia, insulin resistance, and type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    URL: Article
    DOI: 10.3389/fmicb.2022.826487
    DOI: 10.3389/fmicb.2022.826487.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587354-4
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  • 4
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    Data_Sheet_1.docx
    Frontiers Media SA ; 2023
    In:  Frontiers in Microbiology Vol. 14 ( 2023-3-1)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 14 ( 2023-3-1)
    Abstract: The housecleaning enzyme of Mycobacterium tuberculosis (Mtb), MazG, is a nucleoside triphosphate pyrophosphohydrolase (NTP-PPase) and can hydrolyze all canonical or non-canonical NTPs into NMPs and pyrophosphate. The Mycobacterium tuberculosis MazG (Mtb-MazG) contributes to antibiotic resistance in response to oxidative or nitrosative stress under dormancy, making it a promising target for treating TB in latent infection patients. However, the structural basis of Mtb-MazG is not clear. Here we describe the crystal structure of Mtb-MazG (1–185) at 2.7 Å resolution, composed of two similar folded spherical domains in tandem. Unlike other all-α NTP pyrophosphatases, Mtb-MazG has an N-terminal extra region composed of three α-helices and five β-strands. The second domain is global, with five α-helices located in the N-terminal domain. Gel-filtration assay and SAXS analysis show that Mtb-MazG forms an enzyme-active dimer in solution. In addition, the metal ion Mg 2+ is bound with four negative-charged residues Glu119, Glu122, Glu138, and Asp141. Different truncations and site-directed mutagenesis revealed that the full-length dimeric form and the metal ion Mg 2+ are indispensable for the catalytic activity of Mtb-MazG. Thus, our work provides new insights into understanding the molecular basis of Mtb - MazG.
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    URL: Article
    DOI: 10.3389/fmicb.2023.1137279
    DOI: 10.3389/fmicb.2023.1137279.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2587354-4
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  • 5
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    Editorial: Focus on methods: neural algorithms for bio-inspired robotics
    Frontiers Media SA ; 2023
    In:  Frontiers in Neurorobotics Vol. 17 ( 2023-7-25)
    Details
    In: Frontiers in Neurorobotics, Frontiers Media SA, Vol. 17 ( 2023-7-25)
    Type of Medium: Online Resource
    ISSN: 1662-5218
    URL: Article
    DOI: 10.3389/fnbot.2023.1250645
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2453002-5
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  • 6
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    Data_Sheet_1.pdf
    Frontiers Media SA ; 2020
    In:  Frontiers in Cell and Developmental Biology Vol. 8 ( 2020-6-12)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 8 ( 2020-6-12)
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    URL: Article
    DOI: 10.3389/fcell.2020.00408
    DOI: 10.3389/fcell.2020.00408.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2737824-X
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  • 7
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    Data_Sheet_6.docx
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-10-7)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-10-7)
    Abstract: This study aimed to determine whether Bmi-1 deficiency leads to intestinal epithelial barrier destruction and microbiota dysfunction, which members of the microbial community alter barrier function with age, and whether p16 INK4a deletion could reverse the damage of intestinal epithelial barrier and microbial dysbiosis. Intestines from Bmi-1 –deficient ( Bmi-1 –/– ), Bmi-1 and p16 INK4a double-knockout ( Bmi-1 –/– p16 INK4a –/– ), and wild-type mice were observed for aging and inflammation. Duolink Proximity Ligation Assay, immunoprecipitation, and construction of p16 INK4a overexpressed adenovirus and the overexpressed plasmids of full-length, mutant, or truncated fragments for occludin were used for analyzing the interaction between p16 INK4a and occludin. High-throughput sequencing of V4 region amplicon of 16S ribosomal RNA was conducted using intestinal microbiota. We found Bmi-1 deficiency destructed barrier structure, barrier function, and tight junction (TJ) in intestinal epithelium; decreased the TJ proteins; increased tumor necrosis factor α (TNF-α)–dependent barrier permeability; and up-regulated proinflammatory level of macrophages induced by intestinal microbial dysbiosis. The transplantation of fecal microbiota from wild-type mice ameliorated TJ in intestinal epithelium of Bmi-1 –/– and Bmi-1 –/– p16 INK4a –/– mice. Harmful bacteria including Desulfovibrio , Helicobacter , and Oscillibacter were at a higher level in Bmi-1 –/– mice. More harmful bacteria Desulfovibrio entered the epithelium and promoted macrophages-secreted TNF-α and caused TNF-α–dependent barrier permeability and aging. Accumulated p16 INK4a combined with occludin at the 1st–160th residue in cytoplasm of intestinal epithelium cells from Bmi-1 –/– mice, which blocked formation of TJ and the repair of intestinal epithelium barrier. P16 INK4a deletion could maintain barrier function and microbiota balance in Bmi-1 –/– mice through strengthening formation of TJ and decreasing macrophages-secreted TNF-α induced by Desulfovibrio entering the intestinal epithelium. Thus, Bmi-1 maintained intestinal TJ, epithelial barrier function, and microbiota balance through preventing senescence characterized by p16 INK4a accumulation. The clearance of p16 INK4a -positive cells in aging intestinal epithelium would be a new method for maintaining barrier function and microbiota balance. The residues 1–160 of occludin could be a novel therapeutic target for identifying small molecular antagonistic peptides to prevent the combination of p16 INK4a with occludin for protecting TJ.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fcell.2021.671564
    DOI: 10.3389/fcell.2021.671564.s001
    DOI: 10.3389/fcell.2021.671564.s002
    DOI: 10.3389/fcell.2021.671564.s003
    DOI: 10.3389/fcell.2021.671564.s004
    DOI: 10.3389/fcell.2021.671564.s005
    DOI: 10.3389/fcell.2021.671564.s006
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 8
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    Burning alters the decomposition of residual plant litters in Calamagrostis angustifolia wetlands in the Sanjiang Plain (Northeast China)
    Frontiers Media SA ; 2022
    In:  Frontiers in Ecology and Evolution Vol. 10 ( 2022-7-14)
    Details
    In: Frontiers in Ecology and Evolution, Frontiers Media SA, Vol. 10 ( 2022-7-14)
    Abstract: Wetlands store & gt;30% of the global soil carbon pool, which is important for global carbon cycling. However, with global warming and the increase in regional human activities, an increasing number of wetlands are being threatened by fires, which have serious effects on carbon cycling in wetlands. Although plant litter decomposition is one of the key stages of carbon cycling in wetlands, it is still unclear whether fires affect residual plant litter decomposition in burnt wetlands and whether the fire season also causes different effects. To address these knowledge gaps, a plant litter decomposition experiment was conducted during the growing season in autumn burnt, spring burnt, and unburnt sites in a Calamagrostis angustifolia wetland in the Sanjiang Plain (Northeast China). The results show that autumn burning promotes more mass loss (i.e., 15.9 ± 1.6% in autumn burnt sites and 14.8 ± 1.7% in autumn unburnt sites) and accelerates the decomposition of plant litter, whereas spring burning decreases the decomposition rates of plant litter (i.e., 15.7 ± 1.7% in spring burnt sites and 22.0 ± 2.5% in spring unburnt sites). As the decomposition time increased, the accumulation index indicated that carbon was released from plant litter to the surrounding environment accompanied by mass loss and nutrient elements accumulated in the residual plant litter. The N/P ratio of plant litter decreased from ca. 20 on day 26th to ca. 9 on day 121st, indicating that N acts as the limiting element for plant litter decomposition in C. angustifolia wetlands, and the limitation increased with increasing decomposition time. Our results also suggest that the autumn burning may promote more carbon loss and nutrient elements accumulated in plant litter in C. angustifolia wetlands than the spring burning.
    Type of Medium: Online Resource
    ISSN: 2296-701X
    URL: Article
    DOI: 10.3389/fevo.2022.953349
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2745634-1
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  • 9
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    Image4.TIF
    Frontiers Media SA ; 2021
    In:  Frontiers in Molecular Biosciences Vol. 8 ( 2021-7-5)
    Details
    In: Frontiers in Molecular Biosciences, Frontiers Media SA, Vol. 8 ( 2021-7-5)
    Abstract: Isocitrate dehydrogenase (IDH) family of proteins is classified into three subfamilies, namely, types I, II, and III. Although IDHs are widely distributed in bacteria, archaea, and eukaryotes, all type III IDHs reported to date are found only in prokaryotes. Herein, a novel type III IDH subfamily member from the marine microalga Phaeodactylum tricornutum (PtIDH2) was overexpressed, purified, and characterized in detail for the first time. Relatively few eukaryotic genomes encode this type of IDH and PtIDH2 shares the highest homology with marine bacterial monomeric IDHs, suggesting that PtIDH2 originated through a horizontal gene transfer event between a marine alga and a bacterium. Size-exclusion chromatography revealed that the native PtIDH2 is a homotetramer (∼320 kDa) in solution, comprising four monomeric IDH-like subunits (80 kDa each). Enzymatic characterization showed that PtIDH2 is a bivalent metal ion-dependent enzyme and Mn 2+ is the optimal activator. The recombinant PtIDH2 protein exhibited maximal activity at 35°C and pH 8.0 in the presence of Mn 2+ . Heat-inactivation analysis revealed that PtIDH2 is a cold-adapted enzyme. Kinetic analysis demonstrated that PtIDH2 is a completely NADP + -specific IDH with no detectable NAD + -associated catalytic activity. The three putative key NADP + -binding residues (His604, Arg615, and Arg664) in PtIDH2 were also evaluated by site-directed mutagenesis. The H 604 L/R 615 D/R 664 S triple mutant showed a 3.25-fold preference for NAD + over NADP + , implying that the coenzyme specificity of PtIDH2 can be converted from NADP + to NAD + through rational engineering approaches. Additionally, the roles of the conserved residues Ala718 and Leu742 in the thermostability of PtIDH2 were also explored by site-directed mutagenesis. We found that the L 742 F mutant displayed higher thermostability than wild-type PtIDH2. This study expands the phylogeny of the IDH family and provides new insights into the evolution of IDHs.
    Type of Medium: Online Resource
    ISSN: 2296-889X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fmolb.2021.702083
    DOI: 10.3389/fmolb.2021.702083.s001
    DOI: 10.3389/fmolb.2021.702083.s002
    DOI: 10.3389/fmolb.2021.702083.s003
    DOI: 10.3389/fmolb.2021.702083.s004
    DOI: 10.3389/fmolb.2021.702083.s005
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2814330-9
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  • 10
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    Table4.XLSX
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-8-25)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-8-25)
    Abstract: Stroke is a major cause of death and disability throughout the world. A combination of Panax Ginseng and Ginkgo biloba extracts (CGGE) is an effective treatment for nervous system diseases, but the neuroprotective mechanism underlying CGGE remains unclear. Both network analysis and experimental research were employed to explore the potential mechanism of CGGE in treating ischemic stroke (IS). Network analysis identified a total number of 133 potential targets for 34 active ingredients and 239 IS-related targets. What’s more, several processes that might involve the regulation of CGGE against IS were identified, including long-term potentiation, cAMP signaling pathway, neurotrophin signaling pathway, and Nod-like receptor signaling pathway. Our studies in animal models suggested that CGGE could reduce inflammatory response by inhibiting the activity of Nod-like receptor, pyrin containing 3 (NLRP3) inflammasome, and maintain the balance of glutamate (Glu)/gamma-aminobutyric acid (GABA) via activating calmodulin-dependent protein kinase type Ⅳ (CAMK4)/cyclic AMP-responsive element-binding protein (CREB) pathway. These findings indicated the neuroprotective effects of CGGE, possibly improving neuroinflammation and excitotoxicity by regulating the NLRP3 inflammasome and CAMK4/CREB pathway.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fphar.2022.980449
    DOI: 10.3389/fphar.2022.980449.s001
    DOI: 10.3389/fphar.2022.980449.s002
    DOI: 10.3389/fphar.2022.980449.s003
    DOI: 10.3389/fphar.2022.980449.s004
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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