JOURNAL OF MEMBRANE SCIENCE
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2017
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IF 6.035
Libin Yang,Zhan Wang,Jinglong Zhang
The developments of metal organic framework (MOF)/polymer hybrid membranes are hampered by the problems of MOF particles agglomeration and harsh synthetic conditions of MOFs. In this paper, we provide a facile and simple route for fabrication of a uniform MOF/polymer hybrid membrane via the combination of self-assembly and interfacial reaction method. The positive charged polyethyleneimine (PEI) molecules and zinc ions were first deposited on the negative charged hydrolyzed polyacrylonitrile (HPAN) substrate via electrostatic attraction (self-assembly), and then zeolitic imidazolate framework-8 (ZIF-8) particles were in-situ formed in a polyethyleneimine (PEI) layer via interfacial reaction, thereby forming a thin and uniform ZIF-8/PEI hybrid membrane. The prepared membrane possessed a rejection of 99.6% for methyl blue aqueous solutions, with permeance up to 33.0 L m −2 h −1 bar −1 . These results suggested that the ZIF-8/PEI hybrid NF membrane, which was prepared under facile conditions without any complex post-treatment, can be a promising candidate for dye removal process.
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BIOCHEMICAL PHARMACOLOGY
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2016
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IF 5.091
Shan Liu,Lingxin Zhu,Jie Zhang,Jingjing Yu,Xue Cheng,Bin Peng
Previous studies, including those from our laboratory, have demonstrated that the natural flavonoid isoliquiritigenin (ISL) is a promising agent for bone destructive diseases. However, the mechanisms underlying its anti-osteoclastogenic effects are still far from clear. Here, we evaluated the potential alterations of autophagy and nuclear factor-κB (NF-κB) during anti-osteoclastogenic effects by ISL in vitro and in vivo . We observed that ISL inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and suppressed autophagic microtubule-associated protein light chain 3 (LC3)-II and Beclin 1 accumulation. ISL treatment resulted in the interruption of several specific features for autophagy in osteoclast precursors, including acidic vesicular organelle formation, LC3-II accumulation, and appearance of autophagic vacuoles. The RANKL-stimulated expression levels of autophagy-related genes and proteins also diminished in ISL-treated osteoclast precursors. The reactivation of autophagy by rapamycin almost reversed the ISL-elicited anti-osteoclastogenic effects. Interestingly, ISL inhibited the RANKL-stimulated NF-κB expression and nuclear translocation, whereas the NF-κB inhibitor Bay 11-7082 markedly suppressed the RANKL-induced autophagic activation. Consistent with the in vitro results, the administration of ISL could attenuate osteoclastogenic cathepsin K , autophagic LC3, and NF-κB expression to protect against inflammatory calvarial bone erosion in vivo . Our findings highlight the inhibition of NF-κB-dependent autophagy as an important mechanism of ISL-mediated anti-osteoclastogenic activity.
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International Journal of Nanomedicine
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2024
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IF 6.6
Ruijie Wang,Quan Li,Pengxin Wu,Ke Ren,Yan Li,Yang Wang,Huadong Zhu,Chuanzhu Lv
Background In sepsis, the lungs are one of the most severely affected organs, usually resulting in acute lung injury (ALI). Capsaicin (CAP) is a natural compound found in chili peppers that has pain-relieving and anti-inflammatory properties. Here, we report that nanoparticles containing capsaicin and iron (Fe-CAP NPs) exhibited anti-inflammatory effects in the treatment of ALI. Methods The morphological characteristics of nanozymes were detected. RAW 264.7 cells were divided into four groups: control, lipopolysaccharide (LPS), CAP+LPS and Fe-CAP+LPS groups. The expression of inducible nitric oxide synthase (iNOS), transforming growth factor-β (TGF-β), and tumor necrosis factor-α (TNF-α) was assessed by immunofluorescence, Western blot, and enzyme-linked immunosorbent assay (ELISA). Nuclear factor kappa-B (NF-κB) expression was determined by Western blot. C57 mice were divided into control, LPS, CAP+LPS and Fe-CAP+LPS groups. Interleukin-6 (IL-6) and iNOS expression in the lung was detected by Western Blot. IL-6 and TNF-α expression in serum was detected by ELISA. Extravasated Evans blue, histopathological evaluation and wet-to-dry (W/D) weight ratio were used to assess pulmonary capillary permeability. The blood and major organs (heart, liver, spleen, lung and kidney) of mice were tested for the toxicity of Fe-CAP NPs. Results In the LPS group, TNF-α, iNOS, p-NF-κB and p-IKBα expression increased. However, their expression was significantly decreased in the Fe-CAP+LPS group. TGF-β expression showed the opposite trend. In vivo, IL-6 and iNOS expression was notably increased in the lungs of LPS group of mice but decreased with Fe-CAP pretreatment. Fe-CAP significantly ameliorated lung EB leakage, improved the histopathology of lung tissue and reduced the W/D weight ratio. The nanoparticles showed non-cytotoxicity, when studying these biological activities. Conclusion Fe-CAP NPs could alleviated inflammation by inhibiting the expression of pro-inflammatory factors in macrophages, increasing the expression of anti-inflammatory factors, and alleviating lung tissue damage.
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International Heart Journal
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2024
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IF 1.2
Xiaoyu Shen,Jiamei Zhang,Zhou Zhou,Ruiqun Yu
Cardiomyocyte lipotoxicity and ferroptosis are the key to the development of diabetic cardiomyopathy (DCM). Perilipin 5 (PLIN5) is perceived as a significant target of DCM. This study aimed to focus on the role and mechanism of PLIN5 on lipotoxicity and ferroptosis in DCM.Following transfection, mouse cardiomyocytes HL-1 were induced by 0.1 mM palmitic acid (PA) to set up lipotoxic cardiomyocyte models. The cell viability and lipid accumulation were evaluated by cell counting kit-8 assay and Oil red O staining, respectively. Ferrous ion (Fe2+), glutathione (GSH), malondialdehyde (MDA), and reactive oxygen species (ROS) levels were determined to verify the effects of PLIN5 or Pirin (PIR) on ferroptosis. Quantitative real-time reverse transcription polymerase chain reaction or Western blot was performed for quantitative analysis.PLIN5 overexpression promoted the viability, GSH level, and expression of GPX4/PIR/intracellular P65, yet suppressed lipid accumulation, level of Fe2+/MDA/ROS, and expression of interleukin (IL) -1β/IL-18/intranuclear P65 in PA-stimulated HL-1 cells. PIR silencing counteracted the roles of PLIN5 overexpression in PA-stimulated HL-1 cells.PLIN5 suppresses lipotoxicity and ferroptosis in cardiomyocyte via modulating PIR/NF-κB axis, hinting its potential as a therapeutic target in DCM.
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INTERNATIONAL JOURNAL OF HYDROGEN ENERGY
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2024
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IF 8.1
Jing Wang,Min Wang,Zhenjiang Lu,Jing Xie,Jianguo Huang,Jindou Hu,Yali Cao
The inefficient Ni/Fe ion utilization and poor electrical conductivity of nickel-iron layered double hydroxide (NiFe-LDH) restricts to its development in electrocatalytic oxygen evolution reaction/urea oxidation reaction (OER/UOR). Herein, self-supported Hf-doped NiFe-LDH nanosheet arrays were successfully prepared on nickel foam (Hf-NiFe-LDH/NF) via a one-step solvothermal approach for the first time, in which the introduced high-valent Hf 4+ altered the structure of electrons and chemical environment of the atoms and promoted the production of more active sites, thus realizing the fast kinetics of electron transfer on the layer. Meanwhile, the doped metal Hf ions increased the electric conduction and recycling stability of the catalyst. Astoundingly, the overpotential of Hf-NiFe-LDH/NF is barely 258 mV at a current density of 100 mA cm −2 , which is 61 mV lower than that of NiFe-LDH/NF, as well as outstanding stability for over 90 h during the OER. Similarly, the potential is only 1.37 V at 100 mA cm −2 during the UOR, 118 mV less was than at OER. Notably, Hf-NiFe-LDH/NF electrocatalyst exceeds the most previously reported electrocatalysts in terms of performance. This study highlights the benefits of Hf doping strategy in electrocatalytic OER/UOR and presents a promising new type of catalyst for future research.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Yan-Xia Li,Zhong-Fei Zhang,Yu-Meng Wu,Le Shi,Hui-Xian Shen,Navindra P. Seeram,Hang Ma,Yong-Ming Lu
Ashwagandha ( Withania somnifera ) is a well-known medicinal plant, with polysaccharides recognized as key bioactive constituents. In this study, we isolated a neutral polysaccharide, AP-1, from ashwagandha roots and elucidated its structure. AP-1 has a molecular weight of 9.21 kDa and is primarily composed of mannose, glucose, and galactose in a molar ratio of 0.1:1.5:1. Spectroscopic analyses revealed that AP-1's backbone consists of 1,4-α-Glc p and 1,3-α-Gal p , with branching at the C-6 of 1,4,6-α-Glc p and C-4 of 1,3,4-α-Gal p positions. The immunostimulatory activity of AP-1 was evaluated in murine macrophage RAW264.7 cells. AP-1 significantly enhanced macrophage immune responses, promoted M1-type polarization, and activated the NF-κB signaling pathway. It increased the production and mRNAs expression of pro-inflammatory mediators including nitric oxide, oxygen species, tumor necrosis factor, interleukins-1β and -6, and upregulated the M1 surface biomarker CD86. These findings highlight the potential of AP-1 as a promising bioactive ingredient for functional foods targeting immune enhancement.
研究领域:
药用植物学
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免疫学
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生物化学
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Russian Journal of Physical Chemistry A
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2025
·Vol. 99
·期 11
·2797-2808
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IF 0.8
Guangtao Gao,Jiang Zichao,Ma Kaiyue,Chen Qizhi,Liu Huijun
Metal-organic frameworks (MOFs) are widely used as electrode materials due to their porous structure. However, their low conductivity often limits their further development. To overcome the issue, NiCo bimetallic organic framework (NiCo-MOF) and Multiwall carbon nanotube (MWCNT) were attached to Nickel foam (NF) surface without any binder by a simple one-step hydrothermal synthesis, resulting in electrodes with a regular linear layered structure. The structure promoted the electron/ion conduction and exposed more redox active sites, significantly improving electrochemical performance. The electrode prepared with Ni : Co = 1 : 2 and 2% MWCNT exhibited an areal specific capacitance of 5.94 C at 5 mA cm –2 and the capacity retention rate of 83.1% after 5000 cycles at 15 mA cm –2 . The areal-specific capacitance of the modified electrode material increased by nearly 7 times from 0.87 C to 5.94 C cm –2 . Hybrid supercapacitors (HSCs) consisting of the obtained electrodes and activated carbon (AC) had energy density up to 770 mW h cm –2 at a power density of 5.63 W cm –2 .
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MEDIATORS OF INFLAMMATION
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2016
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IF 3.418
Shuai Wang,Zewei Sun,Wenting Zhao,Zhen Wang,Mingjie Wu,Yanyun Pan,Hui Yan,Jianhua Zhu
CD97/ADGRE5 protein is predominantly expressed on leukocytes and belongs to the EGF-TM7 receptors family. It mediates granulocytes accumulation in the inflammatory tissues and is involved in firm adhesion of PMNC on activated endothelial cells. There have not been any studies exploring the role of CD97 in LPS induced NF-κB activation in macrophages. Therefore, we first measured the CD97 expression in LPS treated human primary macrophages and subsequently analyzed the levels of inflammatory factor TNF-α and transcription factor NF-κB in these macrophages that have been manipulated with either CD97 knockdown or overexpression. We found that a reported anti-inflammatory transcription factor, PPAR-γ, was involved in the CD97 mediated NF-κB suppression. Furthermore, by immunofluorescence staining, we established that CD97 overexpression not only inhibited LPS induced p65 expression in the nucleus but also promoted the PPAR-γ expression. Moreover, using CD97 knockout THP-1 cells, we further demonstrated that CD97 promoted PPAR-γ expression and decreased LPS induced NF-κB activation. In conclusion, CD97 plays a negative role in LPS induced NF-κB activation and TNF-α secretion, partly through PPAR-γ upregulation.
研究领域:
免疫学
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细胞生物学
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炎症研究
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INFLAMMATION
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2020
·Vol. 44
·期 2
·645-658
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IF 3.212
Shao Yun-yun,Guo Yao,Feng Xiao-juan,Liu Jun-jin,Chang Zhuang-peng,Deng Gui-feng,Xu Ding,Gao Jian-ping,Hou Rui-gang
To investigate the beneficial effects of oridonin, a diterpenoid compound isolated from Rabdosia rubescens, on the inflammatory response in TNBS-induced post-inflammatory irritable bowel syndrome (PI-IBS) model and the underlying mechanism. Using the PI-IBS rat model and Caco-2 cell lines, we found that intestinal barrier function reflected by lactulose/mannitol (L/M) ratio and tight junction protein level was significantly ameliorated by oridonin. We also demonstrated that oridonin abrogated inflammation through inhibiting the phosphorylation of NF-κBp65 as well as its downstream gene (iNOS, COX-2, IL-1β, and IL-6) level. Molecular docking studies confirmed the good binding activity between oridonin and PXR. In Caco-2 cell lines, oridonin markedly inhibited LPS-induced NF-κB activation in a PXR-dependent manner. Meanwhile, PXR and its target genes CYP3A4 and P-gp were induced by oridonin, which was associated with the decreased expression of NF-κB and the recovery of intestinal barrier. This study indicated that the therapeutic effect of oridonin on experimental PI-IBS through repairing intestinal barrier function may be closely associated with the regulatory role of PXR/NF-κB signaling pathway. Oridonin may serve as a PXR ligand for the development of drugs in the therapy for PI-IBS.
研究领域:
药理学
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胃肠病学
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分子生物学
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细胞生物学
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BIORESOURCE TECHNOLOGY
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2026
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IF 8.2
Qiyao Liu,Wenjiao Sang,Fangzhou Wang,Kai Zhao,Ruiping Liu
Hydrogen, recognized for its high energy density and zero carbon emissions, faces challenges in resource-efficient production. Meanwhile, anaerobic digestion (AD) is frequently impaired by acidification resulting from the accumulation of volatile fatty acids (VFAs), undermining system stability. Herein, we designed a Pt/NF electrode and utilized VFAs-rich acidogenic fermentation liquid as the feedstock for efficient hydrogen production. The electrochemically deposited Pt/NF electrode exhibited excellent hydrogen evolution reaction (HER) activity (overpotential of 340.63 mV at 10 mA/cm 2 ) with high stability. The hydrogen yield of the Pt/NF system was strongly influenced by the applied voltage as well as the type and concentration of VFAs, peaking at 976.20 mL/g CH 3 COOH under conditions of 3.00 V using acetic acid at 5.00 g COD/L. Electrolysis of the actual fermentation liquid produced 28.67 mL of hydrogen and achieved Faradaic and energy efficiencies of 93.92% and 34.77%, respectively, accompanied by an increase in pH and retention of VFAs. hese results demonstrate that the Pt/NF system can be effectively integrated with AD to simultaneously produce green hydrogen and regulate acidification, significantly improving the overall AD process performance and stability.
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Materials Today Bio
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2026
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IF 11
Hongyun Xuan,Zihao Liu,Keyu Lu,Yao Chen,Haonan Gu,Biyun Li,Jingjun Sun,Yan Jin,Yumin Yang,Huihua Yuan
Diabetic wound repair remains a formidable clinical challenge due to impaired healing and heightened infection risks associated with conventional sutures. To address these limitations, this study introduces a novel injectable, self-healing, and antibacterial polysaccharide hydrogel (PGHAA), synthesized from borated peach gum and oxime-modified hyaluronic acid. By leveraging dynamic boronic ester bonds and metal coordination, PGHAA demonstrates enhanced tissue adhesion, self-healing capabilities, and antibacterial activity with immunomodulatory capacity to reprogram chronic wounds into a regenerative state. The incorporation of arginine as a cross-linking agent further improves both biocompatibility and functional performance. In vitro and in vivo evaluations indicate that PGHAA facilitates rapid hemostasis, robust tissue adhesion, and macrophage polarization toward a pro-regenerative phenotype, resulting in accelerated diabetic wound healing. Using an in vivo study with chronic diabetic skin we demonstrated that PGHAA induced wound healing via modulation of IL-17/NF-κB signaling—a pathway repurposed from its classical inflammatory role to drive tissue regeneration. This work redefines diabetic wound therapy by introducing a first-in-class hydrogel that leverages immune modulation for tissue repair, offering a transformative solution for regenerative medicine.
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PHYTOMEDICINE
·
2026
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IF 8.3
Xueling He,Chen Wang,Ruihao Zhang,Yuanyuan Wang,Ying Zhang,Tong Yang,Junzhe Zhang,Shuan Rao,Huan Tang,Xin Peng,Jigang Wang
Background Sepsis, a life-threatening condition, arises from an aberrant or uncontrolled immune response of the host to severe infection. Timely and precise control of this inflammatory response is of paramount importance in sepsis prevention and constitutes the core of sepsis prevention efforts. Parthenolide (PA), recognized as an NF-κB inhibitor, has previously demonstrated its capacity to mitigate the inflammatory response. This study aimed to investigate whether and how PA can inhibit inflammation, thereby alleviating sepsis, and to profile functional target proteins using chemoproteomics strategy. Methods The cecal ligation and puncture (CLP) procedure was performed to induce a mouse model of sepsis, and lipopolysaccharide (LPS) was employed to establish a model of cellular inflammation in mouse mononuclear macrophage cells (RAW264.7) in vitro . Enzyme-linked immunosorbent assay (ELISA) and hematoxylin and eosin (H&E) staining were utilized to evaluate the therapeutic effects of PA on septic mice. In the in vitro experiments, streamlined cysteine activity-based protein profiling (SLC-ABPP) and proteomics techniques were employed to identify potential protein targets and molecular pathways responsible for the anti-inflammatory properties of PA. Results We demonstrated that PA could enhance the survival rate, reduce inflammatory cytokines release, ameliorate histopathological changes, and balance macrophage polarization in a sepsis model. Similarly, PA could effectively alleviate the inflammatory response in LPS-stimulated RAW264.7 cells. Chemoproteomics profiling revealed that Trim33 protein was a potential covalent target of PA via cysteine engagement, and the expression changes of global proteins indicated by proteomics analysis suggested that PA mitigated inflammation by inhibiting the NF-κB pathway. Finally, through a series of molecular biology experiments, we confirmed that PA suppresses the NF-κB pathway by functionally binding to Trim33 and subsequently reducing the ubiquitin dependent degradation of Smad4, thereby exhibiting anti-inflammatory activity. Conclusion Our findings demonstrated that PA significantly mitigated inflammation in sepsis by targeting the Trim33 protein and consequently suppressing ubiquitination on Smad4 as well inhibiting the NF-κB pathway, thus providing new insights into the clinical use of PA in treatment of inflammation related diseases.
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