28 research outputs found

    Fulvic Acid Promotes Legume–Rhizobium Symbiosis by Stimulating Endogenous Flavonoids Synthesis and Secretion

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    Fulvic acid (FA) promotes symbiosis between legumes and rhizobia. To elucidate from the aspect of symbiosis, the effects of root irrigation of water-soluble humic materials (WSHM) or foliar spraying of its highly active component, FA, on soybean root exudates and on rhizosphere microorganisms were investigated. As a result, WSHM/FA treatments significantly altered root exudate metabolite composition, and isoflavonoids were identified as key contributors in both treatments compared to the control. Increased expression of genes related to the isoflavonoid biosynthesis were validated by RT-qPCR in both treatments, which notably elevated the synthesis of symbiotic signals genistein, daidzin, coumestrol, and biochanin A. Moreover, the WSHM/FA treatments induced a change in rhizosphere microbial community, coupled with an increase in the relative abundance of rhizobia. Our findings showed that WSHM/FA promotes symbiosis by stimulating the endogenous flavonoid synthesis and leads to rhizobia accumulation in the rhizosphere. This study provides new insights into mechanisms underlying the FA-mediated promotion of symbiosis

    Fulvic Acid Promotes Legume–Rhizobium Symbiosis by Stimulating Endogenous Flavonoids Synthesis and Secretion

    No full text
    Fulvic acid (FA) promotes symbiosis between legumes and rhizobia. To elucidate from the aspect of symbiosis, the effects of root irrigation of water-soluble humic materials (WSHM) or foliar spraying of its highly active component, FA, on soybean root exudates and on rhizosphere microorganisms were investigated. As a result, WSHM/FA treatments significantly altered root exudate metabolite composition, and isoflavonoids were identified as key contributors in both treatments compared to the control. Increased expression of genes related to the isoflavonoid biosynthesis were validated by RT-qPCR in both treatments, which notably elevated the synthesis of symbiotic signals genistein, daidzin, coumestrol, and biochanin A. Moreover, the WSHM/FA treatments induced a change in rhizosphere microbial community, coupled with an increase in the relative abundance of rhizobia. Our findings showed that WSHM/FA promotes symbiosis by stimulating the endogenous flavonoid synthesis and leads to rhizobia accumulation in the rhizosphere. This study provides new insights into mechanisms underlying the FA-mediated promotion of symbiosis

    Fulvic Acid Promotes Legume–Rhizobium Symbiosis by Stimulating Endogenous Flavonoids Synthesis and Secretion

    No full text
    Fulvic acid (FA) promotes symbiosis between legumes and rhizobia. To elucidate from the aspect of symbiosis, the effects of root irrigation of water-soluble humic materials (WSHM) or foliar spraying of its highly active component, FA, on soybean root exudates and on rhizosphere microorganisms were investigated. As a result, WSHM/FA treatments significantly altered root exudate metabolite composition, and isoflavonoids were identified as key contributors in both treatments compared to the control. Increased expression of genes related to the isoflavonoid biosynthesis were validated by RT-qPCR in both treatments, which notably elevated the synthesis of symbiotic signals genistein, daidzin, coumestrol, and biochanin A. Moreover, the WSHM/FA treatments induced a change in rhizosphere microbial community, coupled with an increase in the relative abundance of rhizobia. Our findings showed that WSHM/FA promotes symbiosis by stimulating the endogenous flavonoid synthesis and leads to rhizobia accumulation in the rhizosphere. This study provides new insights into mechanisms underlying the FA-mediated promotion of symbiosis

    Co-expression of nestin and STAT3 in the reactive astrocytes in the optic nerve after transient intraocular hypertension injury.

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    <p>In control rats, only a few weakly stained nestin-positive cells were observed in the central part of the optic nerve (A,F,K). Nestin-positive signal was seen in the perinuclear cytoplasm and processes of the astrocytes, which showed good co-localization with STAT3 in the same cells (A′,F′,K′). Transient intraocular hypertension induced significant increase of nestin at 3 and 7 days (B–E,G–J,L–O). Strong nestin-positive astrocytes were seen throughout the trans-section of optic nerve (I,J,N,O). Nestin-expressing astrocytes were found co-expressing STAT3 (L,M,N,O,O′).</p

    Expression of STAT3 in the astrocytes of normal and transient intraocular hypertension-injured optic nerve.

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    <p>(A) In control rats, STAT3 immunoreactivity was observed in the processes and perinuclear cytoplasm of astrocyes. STAT3-positive processes connected to form an appearance of honeycomb and partitioned neighboring RGC axons into bundles. Spaces among these axon bundles were perfectly filled by STAT-3 positive cell body. (B) STAT3 showed good co-localization with GFAP in the processes of astrocytes. However, STAT3-positive signal could also be observed at the perinulear cytoplasm, where no GFAP immunoreactivity was found. Therefore STAT3 may give clearer and more entire appearance of the astrocytes than GFAP. (C) From day 3 after the induction of transient intraocular hypertension, STAT3-labeled primary processes of astrocytes in the optic nerve became thicker and tortuous,destroying normal regular honeycomb architecture of the glias. At day 7, hypertrophy of cell soma, thickening of primary processes, and retraction of higher-order processes in STAT3-positive astrocytes were easily identified. The schematic in <b>C</b> depicted how the morphology of STAT3-positive astrocytes changed following transient intraocular hypertension. Quantitative analysis showed that average thickness of STAT3-labeled primary processes was 4.58±0.36 µm at day 7 post-injury compared with 2.68±0.41 µm in normal optic nerve.</p

    Transient intraocular hypertension induced progressive RGC axon loss and structural remodeling of the astrocytes in the optic nerve.

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    <p>(A) Transverse section of control optic nerve was consisted of bundles of tiny and homogeneous RGC axons. From 2 days after the induction of transient intraocular hypertension, progressive axon loss accompanied with fused axonal mass was observed. Quantitative analysis revealed significant decrease in the βIII-tubulin positive area in the cross section of optic nerve at 3 and 7 days. Scar bars, 10 µm. (B) Within normal optic nerve, thin and long primary processes of astrocytes transversely connected with each other to form a honeycomb appearance. These glial tubes segregated neighboring axons into bundles. GFAP and βIII-tubulin double negative spaces were found scattering among the axon bundles, representing the glial cell bodies and vessels. Two days after injury, processes of the astrocytes became much thicker and denser. Spaces among bundles still could be clearly seen. While at 7 days, reactive astrocytes showed hypertrophy and disorganization of their processes. Spaces among bundles were nearly undetectable. Morphological analysis showed that GFAP-positive area in the optic nerve increased gradually following the induction of transient intraocular hypertension and reached statistical significance at 7 days. Scar bars, 50 µm.</p

    Construction of a Switchable Nanochannel for Protein Transport via a Pillar[5]arene-Based Host–Guest System

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    Modulating protein selective translocation is a significant process, which has great potential for mimicking and understanding complex biological activities. As such, how to construct a nanochannel that can accomplish well gating protein transport is vital and challenge. Herein, inspired by nature, we presented a robust strategy to construct a switchable nanochannel by introducing a pH responsive binary host–guest system into a nanochannel. Benefiting from the novel design of the pillar[5]­arene as gatekeeper, the functional nanochannel can well facilitate histone transport. Under pH regulation, the host–guest assembled nanochannel is capable of switching “on” and “off” to manipulate the histone translocation process. This study exemplifies the importance of molecular switch mediated protein transport in this process and provides a new theoretical model for biological research, which will open a new avenue for better understanding of some physiological and pathological behaviors

    Voltage-Responsive Controlled Release Film with Cargo Release Self-Monitoring Property Based on Hydrophobicity Switching

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    Herein, voltage-responsive controlled release film was constructed by grafting ferrocene on the mesoporous inverse opal photonic crystal (mIOPC). The film achieved free-blockage controlled release and realized the monitoring of cargo release without external indicator. Free-blockage was attributed to the voltage switchable nanovalves which undergo hydrophobic-to-hydrophilic transition when applying voltage. Monitoring of cargo release was attributed to the optical property of mIOPC, the bandgap of mIOPC had a red shift when the solution invaded in. The film was hydrophobic enough to stop solution intrusion. Once the voltage was applied, the film became hydrophilic, leading to invasion of the solution. As a result, the cargos were released and the bandgap of mIOPC was red-shifted. Therefore, in this paper both a free-blockage controlled release film and a release sensing system was prepared. The study provides new insights into highly effective controlled release and release sensing without indicator

    DataSheet5_The protective effect of traditional Chinese medicine Jinteng Qingbi granules on rats with rheumatoid arthritis.docx

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    Introduction: Jinteng Qingbi granules (JTQBG), a traditional Chinese medicine formulation, are widely used for the treatment of rheumatoid arthritis (RA) due to their satisfactory therapeutic efficacy. However, the underlying mechanism of action remains unclear. This study aims to investigate the protective effects of JTQBG against RA and elucidates its potential molecular mechanisms.Methods: A collagen-induced arthritis (CIA) rat model was utilized, and JTQBG (1.25, 2.5, 5 g/kg/day) or methotrexate (MTX, 1 mg/kg/week) was orally administered. The rats’ weight, arthritis index (AI), and paw volume were measured weekly. Synovial hyperplasia of the joints was detected using a small animal ultrasound imaging system. Joint destruction was assessed using an X-ray imaging system. Histopathological examinations were performed using hematoxylin-eosin (H&E), Saffron-O and fast green staining. Serum inflammatory cytokines were detected using ELISA. Furthermore, 4D label-free quantitative proteomics of synovial tissues and non-targeted metabolomics of blood serum were conducted to analyze the molecular mechanisms.Results: JTQBG exerted a significant therapeutic effect on CIA rats by reducing inflammatory cell infiltration, synovial hyperplasia, cartilage erosion, and bone destruction. It also decreased the spleen index, inhibited hyperplasia of the white pulp, and decreased the serum levels of IL-1β and IL-18. Proteomics analysis identified 367 differentially expressed proteins (DEPs) between the Model and Normal groups, and 71 DEPs between the JTQBG and Model groups. These DEPs were significantly enriched in the NF-κB pathway. 11 DEPs were significantly reversed after treatment with JTQBG. Western blot results further validated the expression levels of Nfkb1, Pdk1, and Pecam1, and analyzed the expression levels of p-IKK, p-IκBα, and IκBα. The therapeutic efficacy of JTQBG was partly attributed to the suppression of the NF-κB pathway in synovial tissues. Serum metabolomics identified 17 potential biomarkers for JTQBG treatment of CIA rats, which were closely related to Alanine, aspartate and glutamate metabolism, Tryptophan metabolism, Ascorbate and aldarate metabolism, Arginine metabolism, and Inositol phosphate metabolism.Conclusion: Our findings demonstrated that JTQBG was effective against RA by alleviating synovial inflammation, synovial hyperplasia, and joint destruction. The anti-RA properties of JTQBG were likely attributed to the inhibition of the NF-κB pathway and the regulation of serum metabolite disorders.</p

    How β‑Cyclodextrin-Functionalized Biochar Enhanced Biodenitrification in Low C/N Conditions via Regulating Substrate Metabolism and Electron Utilization

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    Biodenitrification plays a vital role in the remediation of nitrogen-contaminated water. However, influent with a low C/N ratio limits the efficiency of denitrification and causes the accumulation/emission of noxious intermediates. In this study, β-cyclodextrin-functionalized biochar (BC@β-CD) was synthesized and applied to promote the denitrification performance of Paracoccus denitrificans when the C/N was only 4, accompanied by increased nitrate reduction efficiency and lower nitrite accumulation and nitrous oxide emission. Transcriptomic and enzymatic activity analyses showed BC@β-CD enhanced glucose degradation by promoting the activities of glycolysis (EMP), the pentose phosphate pathway (PPP), and the tricarboxylic acid (TCA) cycle. Notably, BC@β-CD drove a great generation of electron donors by stimulating the TCA cycle, causing a greater supply of substrate metabolism to denitrification. Meanwhile, the promotional effect of BC@β-CD on oxidative phosphorylation accelerates electron transfer and ATP synthesis. Moreover, the presence of BC@β-CD increased the intracellular iron level, causing further improved electron utilization in denitrification. BC@β-CD helped to remove metabolites and induced positive feedback on the metabolism of P. denitrificans. Collectively, these effects elevated the glucose utilization for supporting denitrification from 36.37% to 51.19%. This study reveals the great potential of BC@β-CD for enhancing denitrification under low C/N conditions and illustrates a potential application approach for β-CD in wastewater bioremediation
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