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JOURNAL OF POWER SOURCES · 2023 · IF 9.2

P vacancies at the crystalline-amorphous interface of NiFe(OH)x/NiPx/NF enhance the catalytic activity of the oxygen evolution reaction

Peng Wang,Tao Yu,Liping Hao,Xuanwen Liu

Efficient electrocatalysts are crucial for overcoming the sluggish kinetics of the oxygen-evolution reaction (OER) and facilitating the advancement of energy storage technologies such as metal-air batteries and hydrogen production through water electrolysis. This study proposes a synergistic approach combining amorphization and interfacial engineering to improve OER performance by fabricating heterojunctions between crystalline NiFe(OH) x and amorphous NiP x . The formation of a strongly coupled crystalline-amorphous heterojunction enables optimization of the electronic structure at the catalytic site and accelerates charge transfer at the interface, thereby improving the reaction kinetics. Notably, we investigate the dynamic adsorption behavior of PO 4 3− during the OER process by introducing Na 3 PO 4 into the electrolyte, revealing that P vacancies serve as active sites in promoting OER activity. Lastly, electrochemical measurements demonstrate that NiFe(OH) x /NiP x /NF exhibits a low overpotential of 220 mV at 10 mA cm −2 and Tafel slope of 35 mV·dec −1 , surpassing the performance of laboratory-prepared noble metal catalysts and most reported NiFe-based electrocatalysts.

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BIOLOGICAL & PHARMACEUTICAL BULLETIN · 2021 ·Vol. 44 ·期 8 ·1093-1100 · IF 2.233

Hydrogen Sulfide Improves Functional Recovery in Rat Traumatic Spinal Cord Injury Model by Inducing Nuclear Translocation of NF-E2-Related Factor 2

Chang Xu,Man Zhang,Guangping Zhang,Sheng Yan,Weiqi Yan

Hydrogen sulfide (H2S), an important gaseous messenger, is known to have neuroprotective effects in many neurological disorders. This study examined the neuroprotective effects and the associated mechanisms of H2S in the model Sprague–Dawley (SD) rats with spinal cord injury (SCI). We found that H2S showed neuroprotective effects in SCI model rats, improved the symptoms of neurological impairment, reduced the secretion of inflammatory factors, nerve cell apoptosis, and endoplasmic reticulum (ER), and oxidative stresses. Moreover, these effects were produced by activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) protein. Our results suggest that H2S supplementation could be a potential therapeutic strategy to promote SCI recovery.

✓ 已验证 DOI PubMed 高影响因子
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Environmental Science-Water Research & Technology · 2021 ·Vol. 7 ·期 5 ·956-968 · IF 4.251

A facile and economic route assisted by trace tannic acid to construct a high-performance thin film composite NF membrane for desalination

Na Zhang,Xiangju Song,Yiqiang Chen,Bin Jiang,Luhong Zhang,Heqing Jiang

Tailoring the structure and properties of the polyamide (PA) layer in a straightforward way is considered promising for fabricating advanced thin film composite (TFC) nanofiltration (NF) membranes. Herein, green and cost-effective tannic acid (TA) was used as an effective additive in the aqueous phase to construct TFC NF membranes via interfacial polymerization (IP) of piperazine (PIP) and trimesoyl chloride (TMC). It was found that the introduction of a small quantity of TA could alter the IP process by attracting more PIP monomers, locally enriching them on the substrate and hindering their diffusion toward the water/organic interface via protonation reaction and hydrogen bonding, resulting in a rough and dense PA structure. Besides, characterizations confirmed that the proper incorporation of TA improved the membrane cross-linking degree, surface hydrophilicity and electronegativity. Consequently, the optimal TFC membrane, obtained at a low TA concentration of 0.004 w/v%, exhibited superior separation performance with permeate fluxes of 67.1 LMH and 55.7 LMH and rejections of 97.0% and 94.4% for Na2SO4 and MgSO4 solutions, respectively. Notably, the optimized TFC membrane outperformed its control counterparts, indicating the efficiency of TA incorporation in constructing a high-performance TFC NF membrane. This work provides a straightforward and economic route to fabricate competitive dense NF membranes for water purification.

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Journal of Neuroinflammation · 2019 ·Vol. 16 ·期 1 ·1-13 · IF 5.7

NDP-MSH binding melanocortin-1 receptor ameliorates neuroinflammation and BBB disruption through CREB/Nr4a1/NF-κB pathway after intracerebral hemorrhage in mice

Wu Xuan,Fu Siming,Liu Yun,Luo Hansheng,Li Feng,Wang Yiying,Gao Meng,Cheng Yuan,Xie Zongyi

Background Neuroinflammation and blood-brain barrier (BBB) disruption are two vital mechanisms of secondary brain injury following intracerebral hemorrhage (ICH). Recently, melanocortin-1 receptor (Mc1r) activation by Nle4-D-Phe7-α-MSH (NDP-MSH) was shown to play a neuroprotective role in an experimental autoimmune encephalomyelitis (EAE) mouse model. This study aimed to investigate whether NDP-MSH could alleviate neuroinflammation and BBB disruption after experimental ICH, as well as the potential mechanisms of its neuroprotective roles.Methods Two hundred and eighteen male C57BL/6 mice were subjected to autologous blood-injection ICH model. NDP-MSH, an agonist of Mc1r, was administered intraperitoneally injected at 1 h after ICH insult. To further explore the related protective mechanisms, Mc1r small interfering RNA (Mc1r siRNA) and nuclear receptor subfamily 4 group A member 1 (Nr4a1) siRNA were administered via intracerebroventricular (i.c.v) injection before ICH induction. Neurological test, BBB permeability, brain water content, immunofluorescence staining, and Western blot analysis were implemented.Results The Expression of Mc1r was significantly increased after ICH. Mc1r was mainly expressed in microglia, astrocytes, and endothelial cells following ICH. Treatment with NDP-MSH remarkably improved neurological function and reduced BBB disruption, brain water content, and the number of microglia in the peri-hematoma tissue after ICH. Meanwhile, the administration of NDP-MSH significantly reduced the expression of p-NF-κB p65, IL-1β, TNF-α, and MMP-9 and increased the expression of p-CREB, Nr4a1, ZO-1, occludin, and Lama5. Inversely, the knockdown of Mc1r or Nr4a1 abolished the neuroprotective effects of NDP-MSH.Conclusion sTaken together, NDP-MSH binding Mc1r attenuated neuroinflammation and BBB disruption and improved neurological deficits, at least in part through CREB/Nr4a1/NF-κB pathway after ICH.

CAS / MDL: 314-13-6
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CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY · 2019 ·Vol. 46 ·期 12 ·1194-1200 · IF 2.336

Platycodin D inhibits proliferation, migration and induces chemosensitization through inactivation of the NF-κB and JAK2/STAT3 pathways in multiple myeloma cells

Di Wu,Wei Zhang,Ying Chen,Hong Ma,Mengchang Wang

Multiple myeloma (MM) is a malignancy characterized by the proliferation of malignant plasma cells. Platycodin D (PLD) is a triterpenoid saponin that exerts anti-tumour activity through multiple mechanisms. However, the role of PLD in MM remains unknown. Here, we investigated the effect of PLD on MM cell lines NCI-H929 and U266B1, and elucidated the underlying molecular mechanism. Cell Counting Kit-8 assay showed that the proliferation of NCI-H929 and U266B1 cells was significantly decreased after PLD treatment. Transwell assay confirmed that PLD treatment suppressed migration of NCI-H929 and U266B1 cells. Flow cytometry results indicated that the apoptotic rates of bortezomib (BTZ)-treated NCI-H929 and U266B1 cells were markedly increased after PLD treatment. Western blot analysis revealed that bcl-2 expression was decreased, while bax expression was increased in PLD-treated NCI-H929 and U266B1 cells compared with that in BTZ-treated cells. Furthermore, PLD treatment blocked the activation of nuclear factor-kappa B (NF-κB) and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signalling pathways in NCI-H929 cells. Taken together, these data showed that PLD inhibited proliferation and migration, and enhanced chemosensitization to BTZ through inactivation of the NF-κB and JAK2/STAT3 pathways in MM cell lines. These findings indicated that PLD might serve as a novel therapeutic agent for the treatment of MM.

✓ 已验证 DOI PubMed 高影响因子
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BASIC RESEARCH IN CARDIOLOGY · 2016 ·Vol. 112 ·期 1 ·1-15 · IF 6.038

MD2 mediates angiotensin II-induced cardiac inflammation and remodeling via directly binding to Ang II and activating TLR4/NF-κB signaling pathway

Han Jibo,Zou Chunpeng,Mei Liqin,Zhang Yali,Qian Yuanyuan,You Shengban,Pan Yong,Xu Zheng,Bai Bin,Huang Weijian,Liang Guang

Angiotensin II (Ang II) induces cardiac inflammation and remodeling. Emerging evidence indicates that Ang II may utilize the Toll-like receptor 4 (TLR4) signaling pathway in mediating pro-inflammatory and pro-fibrotic activities. However, the precise mechanism is poorly understood. Myeloid differentiation 2 (MD2), a molecule that physically binds to TLR4, confers lipopolysaccharide responsiveness and may also be involved in mediating the actions of Ang II. We hypothesize that MD2 plays an essential role in cardiac inflammation and remodeling induced by local Ang II, and inhibition of MD2 can attenuate Ang II-induced cardiac dysfunction. Using a specific small molecule MD2 blocker L6H21 and the MD2 knockout mice, we show that MD2 deficiency significantly reduces cardiac inflammation and subsequent fibrosis, hypertrophy, and dysfunction in mice challenged with subcutaneous injection of Ang II. In rat cardiomyocyte-like H9c2 cells as well as rat primary cardiomyocytes, inhibition of MD2 by L6H21 or siRNA knockdown suppressed the Ang II-induced TLR4 signaling pathway activation including MyD88 recruitment, and reduced cardiomyocyte hypertrophy and matrix protein expression. These pro-inflammatory activities of Ang II were independent of the AT1 receptor. Finally, we demonstrated the direct interaction between Ang II and MD2 protein via hydrogen bonds on Arg-90, Glu-92, and Asp-100. Ang II produces an inflammatory response and cardiac remodeling by directly binding to MD2, activating MD2/TLR4 complex, and recruiting MyD88. MD2 may be a new therapeutic target for Ang II-mediated cardiac inflammation and remodeling.

CAS / MDL: 1405-20-5
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CARBOHYDRATE POLYMERS · 2024 · IF 10.7

Composite microneedles loaded with Astragalus membranaceus polysaccharide nanoparticles promote wound healing by curbing the ROS/NF-κB pathway to regulate macrophage polarization

Xiaowei Liu,Chunjing Guo,Weili Yang,Wenxin Wang,Ningning Diao,Min Cao,Yuxin Cao,Xuemei Wang,Xinxin Wang,Huijie Pei,Yifan Jiang,Ming Kong,Daquan Chen

The healing of chronic diabetic wounds remains a formidable challenge in modern times. In this study, a novel traditional Chinese medicine microneedle patch was designed based on the physiological characteristics of wounds, with properties including hemostasis, anti-inflammatory, antioxidant, antimicrobial, and induction of angiogenesis. Initially, white peony polysaccharide (BSP) with hemostatic properties and carboxymethyl chitosan (CMCS) with antimicrobial capabilities were used as materials for microneedle fabrication. To endow it with antimicrobial, procoagulant, and adhesive properties. Among them, loaded with ROS-sensitive nanoparticles of Astragalus polysaccharides (APS) based on effective components baicalein (Bai) and berberine (Ber) from Scutellaria baicalensis (SB) and Coptis chinensis (CC) drugs (APB@Ber). Together, they are constructed into multifunctional traditional Chinese medicine composite microneedles (C/B@APB@Ber). Bai and Ber synergistically exert anti-inflammatory and antimicrobial effects. Microneedle patches loaded with BSP and APS exhibited significant effects on cell proliferation and angiogenesis induction. The combination of composite polysaccharides enabled the microneedles to adhere stably to wounds and provide sufficient strength to penetrate the biofilm and induce dispersion. The combination of composite polysaccharides enabled the microneedles to adhere stably to wounds and provide sufficient strength to penetrate the biofilm and induce dispersion. Therefore, traditional Chinese medicine multifunctional microneedle patches offer potential medical value in promoting the healing of diabetic wounds.

CAS / MDL: 13718-50-8
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY · 2024 · IF 5.7

Enteromorpha prolifera Polysaccharide Alleviates Acute Alcoholic Liver Injury in C57 BL/6 Mice through the Gut–Liver Axis and NF-κB Pathway

Tingting Yan,Jinghe Sun,Yuying Zhang,Chengrong Wen,Jingfeng Yang

Enteromorpha prolifera polysaccharide (EP2) protection against acute alcoholic liver injury (AALI) in mice was investigated. By integration of physiological indicators, gut microbiota, and short-chain fatty acids (SCFAs), the mechanism of EP2 in alleviating AALI was disclosed. The results showed that EP2 significantly ameliorated alcohol-induced abnormal transaminase activities, liver and intestinal systemic inflammation, and intestinal environmental disorders. EP2 significantly reduces liver and serum LPS contents by 1.69-fold and 1.54-fold. Furthermore, inhibition of the NF-κB signaling pathway by EP2 reduced the production of proinflammatory cytokines such as TNF-α (1.83-fold), IL-6 (11.09-fold), and IL-1β (1.99-fold). EP2 restored SCFAs to normal levels by upregulating the abundance of beneficial bacteria (Colidextribacter, Ruminococcus, unclassified_Lachnospiraceae, and Akkermansia). The alleviation of AALI by EP2 occurs through protection of the intestinal mucosal barrier and reduction of LPS permeating in serum. The decrease in LPS inactivates the NF-κB signaling pathway and prevents inflammation. In short, EP2 regulates the gut–liver axis and inflammation, alleviating effects in AALI mice.

CAS / MDL: 631-61-8
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JOURNAL OF ETHNOPHARMACOLOGY · 2025 · IF 5.4

Ginsenoside Rb1 alleviates blood-brain barrier damage and demyelination in experimental autoimmune encephalomyelitis mice by regulating JNK/ ERK/NF-κB signaling pathway

Yingying Song,Xiaojuan Zhang,Xinyan Han,Gaorui Wang,Mengxue Wang,Hui Wu,Xiaojun Wu

Ethnopharmacological relevance The traditional Chinese herb Panax ginseng recorded in "Shennong Herbal Classic" is renowned for its purported vascular regulatory properties and immune-enhancing capabilities. Ginsenoside Rb1 (Rb1), a prominent bioactive compound in Panax, has demonstrated significant neuropharmacological activities. However, its impact on multiple sclerosis (MS) and blood-brain barrier (BBB) damage remains inadequately investigated. Aim of the study Inflammation and BBB disruption are pivotal to MS. Tightly packed brain capillary endothelial cells are fundamental to the structural and functional integrity of the BBB. Rb1 has been shown to alleviate BBB damage in stroke rats, but its effect on BBB damage in MS is not well understood. The objective of this study was to examine the role and mechanism of Rb1 on BBB injury in experimental autoimmune encephalomyelitis (EAE) mice. Materials and methods The BBB protection effect and mechanism of Rb1 were evaluated in LPS-treated bEnd.3 cells and EAE model mice. The mRNA expression levels of the inflammatory factor and the protein expressions of matrix metalloproteinases 9 (MMP9), zona occludens 1 (ZO-1), inhibitor of NF-κB (IκBα), occludin, Jun-amino-terminal kinase (JNK), and nuclear factor-κB (NF-κB) in bEnd.3 cells and mouse cerebral cortex were quantified. The permeability of bEnd.3 cells was examined by measuring trans-endothelial electrical resistance (TEER) and sodium fluorescein (NaF) leakage. Results Rb1 administration in the early stages of EAE postponed the disease's onset and lessened its severity. Rb1 inhibited the destruction of the BBB in brain cortex of EAE mice. Rb1 reduced the lipopolysaccharide (LPS)-induced hyperpermeability of bEnd.3 cells and prevented the downregulation of TJ proteins. In addition, in LPS-induced bEnd.3 cells, Rb1 decreased the overproduction of reactive oxygen species. Moreover, Rb1 suppressed the phosphorylation of JNK, ERK, NF-κB, and IκB in vivo and in vitro. Furthermore, the JNK agonist anisomycin was observed to partially abolish the protective effect of Rb1 in bEnd.3 cells treated with LPS. Conclusions Taken together, we demonstrated that Rb1 improved demyelination and BBB damage in EAE mice by modulating JNK/ERK/NF-κB signaling pathway. This study can offer a theoretical foundation for the use of Rb1 in the treatment of EAE by preventing BBB injury.

CAS / MDL: 76-03-9
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JOURNAL OF MEMBRANE SCIENCE · 2024 · IF 8.4

How to understand the effect of relative humidity on the morphology and performance of polypiperazine-amide NF membrane during heat curing process

Ke Xiang,Zhen-Liang Xu,Yong-Jian Tang

Recent studies have shown that the temperature and time of the heat curing process have important effects on the nanofiltration (NF) membrane structure and properties. However, the mechanism of the relative humidity (RH), as one of the important factors in the heat curing of NF membranes, is still unclear. To analyze the specific effect of RH, we compared the heat curing results of the NF polyamide (PA) membranes fabricated with different monomer concentrations at various RH. The nanofiltration performance of the membranes appeared to be non-uniform when the RH was in the range of 40 %–60 %. Within the appropriate RH range , the rejection of Na 2 SO 4 was preserved at about 98.5 % for the manufactured NF membranes. At high concentrations, the increasing RH created a discontinuous condensate layer on the PA layer surface, which affected the morphology and physicochemical properties of the NF membrane causing a doubling of pure water permeability (PWP) to 8.33 L m −2  h −1 ·bar −1 . At low concentrations, the PA layer was not significantly changed with the increase of RH, but the evaporation of water from the smaller capillary pores in its PES substrate was slowed down, which reduced the capillary stress on the substrate and prevented the collapse of the substrate pore size, resulting in a nearly 20 times increase in its PWP to 39.7 L m −2  h −1 ·bar −1 . This work reveals the effect of RH during heat curing and gives significant guidance to the design and synthesis of high-performance NF membranes.

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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS · 2025 · IF 5.4

1D FeS-Ni3S2/NF nanocatalysts with rigid polysulfide segment as sulfur source and in situ intercalator for enhanced oxygen evolution reaction activity

Qian Zhao,Jianlong Gou,Mengxinyue Zhang,Hong Chen,Guiyu Zhu,Xiaoxiao Zhang,Yanan Xue,Yanping Liu,Jianzhi Wang

Developing sulfur-containing one-dimensional (1D) nanocatalysts with high active surface area and stability remains a significant challenge for achieving high-performance oxygen evolution reaction (OER) catalysts. In this study, a novel 1D FeS-Ni 3 S 2 nanorod array covered with interwoven nanosheets was synthesized on nickel foam (NF) using a solvothermal process. A rigid segment-containing polysulfide (Poly(S- r -DIB)) was employed as a sulfur source and in situ intercalator, enabling efficient sulfidation and structural formation. The resulting FeS-Ni 3 S 2 /NF nanocatalyst demonstrated outstanding OER performance, achieving a low overpotential of 215 mV at 50 mA cm - ² and a low Tafel slope of 51 mV dec - ¹ . The catalyst exhibited remarkable stability, retaining over 85 % of its original activity after prolonged testing. Furthermore, in a two-electrode configuration, the catalyst reached a current density of 20 mA cm - ² at a low applied voltage of 1.41 V. This work introduces a new approach for fabricating sulfur-containing 1D nanomaterials with superior catalytic activity, paving the way for advancements in water splitting and sustainable hydrogen energy production.

CAS / MDL: 12036-10-1 7647-01-0
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Journal of Translational Medicine · 2024 ·Vol. 22 ·期 1 ·1-19 · IF 6.1

Synergistic effect of mesenchymal stem cell-derived extracellular vesicle and miR-137 alleviates autism-like behaviors by modulating the NF-κB pathway

Qin Qian,Shan Zhiyan,Xing Lei,Jiang Yutong,Li Mengyue,Fan Linlin,Zeng Xin,Ma Xinrui,Zheng Danyang,Wang Han,Wang Hui,Liu Hao,Liang Shengjun,Wu Lijie,Liang Shuang

Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental disorder predominant in childhood. Despite existing treatments, the benefits are still limited. This study explored the effectiveness of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) loaded with miR-137 in enhancing autism-like behaviors and mitigating neuroinflammation. Utilizing BTBR mice as an autism model, the study demonstrated that intranasal administration of MSC-miR137-EVs ameliorates autism-like behaviors and inhibits pro-inflammatory factors via the TLR4/NF-κB pathway. In vitro evaluation of LPS-activated BV2 cells revealed that MSC-miR137-EVs target the TLR4/NF-κB pathway through miR-137 inhibits proinflammatory M1 microglia. Moreover, bioinformatics analysis identified that MSC-EVs are rich in miR-146a-5p, which targets the TRAF6/NF-κB signaling pathway. In summary, the findings suggest that the integration of MSC-EVs with miR-137 may be a promising therapeutic strategy for ASD, which is worthy of clinical adoption.

CAS / MDL: 100068-60-8
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