BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2018
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IF 2.559
Fan Zhang,Chenhong Zhang
Intracerebral hemorrhage (ICH) is reported as a common and often fatal type of stroke accompanied with high morbidity and mortality, and it frequently results in long-lasting neurological dysfunctions. However, the pathogenesis that contributes to ICH has not been fully understood. Rnf112, also known as Znf179, is a member of the RING finger protein family. The expression of Rnf112 is abundant in the brain and is modulated during brain progression and development. The study aimed to explore the role of Rnf112 in brain injury after ICH, as well as the underlying molecular mechanisms. The results indicated that ICH led to a significant decrease in Rnf112, which was confirmed in oxyhemoglobin (oxyHb)-incubated astrocytes and microglial cells. Moreover, the Rnf112 knockout (Rnf112 −/− ) mice and wild type (WT) mice induced by ICH were further employed. Compared to the WT/ICH group, Rnf112 −/− mice exhibited accelerated brain injury, as evidenced by the increased brain water contents and neurological deficit scores (NDS). In comparison to WT/ICH group, a remarkable up-regulation in the release of pro-inflammatory cytokines, including tumor necrotic factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β, was observed in perihematoma tissues of Rnf112 −/− mice on day 3 post-ICH. The process was along with promoted glial fibrillary acidic protein (GFAP) and Iba1 expression and reduced NeuN levels. Furthermore, ICH-induced increases in toll-like receptor (TLR)-4 and myeloid differentiation primary response protein (MyD88) expression were exacerbated by the loss of Rnf112. The phosphorylated expression of IKKα, inhibitor of NF-κB (IκBα) and nuclear factor-kappa B (NF-κB) induced by ICH in perihematoma tissues of mice was markedly enhanced in Rnf112 −/− mice. Rnf112 repression-induced inflammatory response was verified in lipopolysaccharide (LPS)-incubated glial cells . In contrast, over-expressing Rnf112 markedly attenuated ICH-induced brain injury by restraining inflammation via inactivating TLR-4/NF-κB pathway. In summary, our findings suggested that Rnf112 expression was highly involved in the progression of ICH, and targeting Rnf112 signaling might be a promising therapeutic strategy against ICH development.
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RSC Advances
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2018
·Vol. 8
·期 51
·29455-29463
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IF 2.936
Hai-Zhen Zhang,Zhen-Liang Xu,Jing-Ying Sun
Nanofiltration (NF) membranes with simultaneous high rejection of divalent cations and anions and high water permeation were designed and fabricated via interfacial polymerization (IP) on three-channel capillary ultrafiltration (UF) membranes. MWCNTs-COOH were modified with poly(amidoamine) (PAMAM) and the as-synthesized MWCNTs-PAMAM were embedded into the inner polyamide skin-layer of the NF membranes by incorporating them into a piperazine (PIP) aqueous solution, followed by IP with trimesoyl chloride (TMC). The rigid MWCNTs and the dendrimer PAMAM molecules endow the as-fabricated NF membranes with high porosity and good hydrophilicity. Additionally, the –NH2 groups of PAMAM introduce some positive sites into the polyamide layer. The as-prepared NF membranes with incorporated MWCNTs-PAMAM exhibit a pure water flux of 48.7 L m−2 h−1 and 92.6% and 88.5% rejection for Na2SO4 and MgCl2, respectively, at 4 bar. Moreover, the NF membranes display high rejection for sulfates and metal cations, including heavy metal ions. The practicability of the membranes for mine-wastewater treatment was tested, and the membranes showed above 80% rejection of heavy metals and solution flux of about 30 L m−2 h−1. In addition, their separation performance and stability were satisfactory during the long-term run. The high rejection of the membranes for metal cations is ascribed to the positive sites offered by MWCNTs-PAMAM and the narrow membrane pores since both electrostatic repulsion and size exclusion play a role during membrane filtration. The good separation performance of the membranes for multivalent anions and heavy metal cations illustrates their potential for applications in heavy metal wastewater treatment.
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INTERNATIONAL JOURNAL OF HYDROGEN ENERGY
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2017
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IF 3.582
Lirong Huang,Yanping Hou,Zebin Yu,Zhenbo Peng,Li Wang,Jun Huang,Boge Zhang,Lun Qian,Leidan Wu,Zongchen Li
The electrode with high catalytic activity , low hydrogen overpotential and low cost is desired for hydrogen evolution reaction (HER) via electrocatalytic water splitting. In this study, Pt/Fe-Ni foam (Pt/Fe-NF) electrode was synthesized via cathodic electrodeposition followed by impregnation deposition. Physical and electrochemical properties of Pt/Fe-NF, NF and Pt/NF electrodes were characterized by various techniques. The Pt/Fe-NF electrode exhibited better electrochemical activity for HER under alkaline condition than those of Pt/NF and NF electrodes, owing to the introduction of zero valences Pt and Fe onto the NF, and synergetic effect resulted from the formation of Fe-Ni alloy. Furthermore, Pt/Fe-NF electrode showed extremely high double-layer capacitance (69.1 mFcm −2 ), suggesting high active sites for the Pt/Fe-NF. Tafel slope of Pt/Fe-NF was 59.9 mV dec −1 , indicating that the Volmer-Heyrovsky HER mechanism was the rate-limiting step. The Pt/Fe-NF electrode with great electrocatalytic activity is a promising electro-catalyst for industrial hydrogen production from alkaline electrolyte .
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BIOMATERIALS
·
2017
·
IF 8.402
Qin Wang,Hao Jiang,Yan Li,Wenfei Chen,Hanmei Li,Ke Peng,Zhirong Zhang,Xun Sun
The transcription factor NF-kB plays a pivotal role in the pathogenesis of rheumatoid arthritis. Here we attempt to slow arthritis progression by co-delivering the glucocorticoid dexamethasone (Dex) and small-interfering RNA targeting NF-kB p65 using our previously developed polymeric hybrid micelle system. These micelles contain two similar amphiphilic copolymers : polycaprolactone-polyethylenimine (PCL-PEI) and polycaprolactone-polyethyleneglycol (PCL-PEG). The hybrid micelles loaded with Dex and siRNA effectively inhibited NF-kB signaling in murine macrophages more efficiently than micelles containing either Dex or siRNA on their own. In addition, the co-delivery system was able to switch macrophages from the M1 to M2 state. Injecting hybrid micelles containing Dex and siRNA into mice with collagen-induced arthritis led the therapeutic agents to accumulate in inflamed joints and reduce inflammation, without damaging renal or liver function. Thus, blocking NF-kB activation in inflammatory tissue using micelle-based co-delivery may provide a new approach for treating inflammatory disease.
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EXPERIMENTAL ANIMALS
·
2024
·
IF 2.2
Zhi-Hui GUAN,Di YANG,Yi WANG,Jia-Bin MA,Guo-Nian WANG
Ischemia/reperfusion (I/R) is a pathological process that occurs in numerous organs and is often associated with severe cellular damage and death. Ectodysplasin-A2 receptor (EDA2R) is a member of the TNF receptor family that has anti-inflammatory and antioxidant effects. However, to the best of our knowledge, its role in the progression of myocardial I/R injury remains unclear. The present study aimed to investigate the role of EDA2R during myocardial I/R injury and the molecular mechanisms involved. In vitro, dexmedetomidine (DEX) exhibited a protective effect on hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury and downregulated EDA2R expression. Subsequently, EDA2R silencing enhanced cell viability and reduced the apoptosis of cardiomyocytes. Furthermore, knockdown of EDA2R led to an elevated mitochondrial membrane potential (MMP), repressed the release of Cytochrome C and upregulated Bcl-2 expression. EDA2R knockdown also resulted in downregulated expression of Bax, and decreased activity of Caspase-3 and Caspase-9 in cardiomyocytes, reversing the effects of H/R on mitochondria-mediated apoptosis. In addition, knockdown of EDA2R suppressed H/R-induced oxidative stress. Mechanistically, EDA2R knockdown inactivated the NF-κB signaling pathway. Additionally, downregulation of EDA2R weakened myocardial I/R injury in mice, as reflected by improved left ventricular function and reduced infarct size, as well as suppressed apoptosis and oxidative stress. Additionally, EDA2R knockdown repressed the activation of NF-κB signal in vivo. Collectively, knockdown of EDA2R exerted anti-apoptotic and antioxidant effects against I/R injury in vivo and in vitro by suppressing the NF-κB signaling pathway.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Cheng Lu,ShiJun Deng,YanJiao Liu,ShengJin Yang,DingMei Qin,LiJuan Zhang,Rui-rui Wang,Yi Zhang
Available online Atopic dermatitis (AD) is a chronic, persistent inflammatory skin disease characterized by eczema-like lesions and itching. Although topical steroids have been reported for treating AD, they are associated with adverse effects. Thus, safer medications are needed for those who cannot tolerate these agents for long periods. Mangiferin (MAN) is a flavonoid widely found in many herbs, with significant anti-inflammatory and immunomodulatory activities. However, the potential modulatory effects and mechanisms of MAN in treating Th2 inflammation in AD are unknown. In the present study, we reported that MAN could reduce inflammatory cell infiltration and scratching at the lesion site by decreasing MC903-induced levels of Th2-type cytokines, Histamine, thymic stromal lymphopoietin, Leukotriene B4, and immunoglobulin E. The mechanism may be related to reductions in MAPK and NF-κB-associated protein phosphorylation by macrophages. The results suggested that MAN may be a promising therapeutic agent for AD.
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ELECTROCHIMICA ACTA
·
2025
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IF 5.6
Xuewei Ba,Xinyu Lan,Huaikang Zhang,Cheng Cheng,Wenping Huang,Xinyu Han,Deqing Zhang,Yan Yu
Transition metal compounds have garnered significant attention due to their high specific surface area, tunable composition, and synergistic effects. These materials exhibit excellent electrochemical performance, making them some of the most promising candidates for pseudocapacitive applications. Herein, cobalt selenide (CoSe), nickel selenide (NiSe), and trinickel diselenide (Ni 3 Se 2 ) nanosheets were grown on nickel foam using a simple two-step hydrothermal method. The three-dimensional network structure of the CoSe/NiSe/Ni 3 Se 2 @NF composite material provides a larger specific surface area and more electrochemically active sites. This architecture facilitates rapid electron transfer, enhances electrochemical performance, and results in a high specific capacitance of 2300.65 F· g −1 at a current density of 1 A· g −1 . The asymmetric supercapacitor device, assembled with CoSe/NiSe/Ni 3 Se 2 @NF as the positive electrode and activated carbon as the negative electrode, demonstrates an energy density of 63.16 Wh·kg −1 at a power density of 805.73 W·kg −1 . These outstanding electrochemical properties suggest that CoSe/NiSe/Ni 3 Se 2 @NF composite materials hold great potential as an energy storage material.
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PHYTOMEDICINE
·
2024
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IF 6.7
Pingping Tuo,Risheng Zhao,Ning Li,Shuang Yan,Gege Yang,Chunmei Wang,Jinghui Sun,Haiming Sun,Mengyang Wang
Background Ang II induces hypertensive heart failure (HF) via hemodynamic and non-hemodynamic actions. Lycorine (LYC) is an alkaloid derived from Lycoris bulbs, and it possesses anti-cardiovascular disease-related activities. Herein, we explored the potential LYC-mediated regulation of Ang II-induced HF. Methods Over 4 weeks, we established a hypertensive HF mouse model by infusing Ang II into C57BL/6 mice using a micro-osmotic pump. For the final two weeks, mice were administered LYC via intraperitoneal injection. The LYC signaling network was then deduced using RNA sequencing. Results LYC administration strongly suppressed hypertrophy, myocardial fibrosis, and cardiac inflammation. As a result, it minimized heart dysfunction while causing no changes in blood pressure. The Nuclear Factor kappa B (NF-κB) network/phosphoinositol-3-kinase (PI3K)-protein kinase B (AKT) was found to be a major modulator of LYC-based cardioprotection using RNA sequencing study. We further confirmed that in cultured cardiomyocytes and mouse hearts, LYC reduced the inflammatory response and downregulated the Ang II-induced PI3K-AKT/NF-κB network. Moreover, PI3K-AKT or NF-κB axis depletion in cardiomyocytes completely abrogated the anti-inflammatory activities of LYC. Conclusion Herein, we demonstrated that LYC safeguarded hearts in Ang II -stimulated mice by suppressing the PI3K-AKT/NF-κB-induced inflammatory responses. Given the evidence mentioned above, LYC is a robust therapeutic agent for hypertensive HF.
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Frontiers in Pharmacology
·
2025
·
IF 4.8
Yancen Li,Chengyu Wan,Fan Li,Guang Xin,Tao Wang,Qilong Zhou,Tingyu Wen,Shiyi Li,Xiaoting Chen,Wen Huang
Background: Isatidis Folium, a botanical drug widely used in traditional medicine, is known for its anti-inflammatory properties, including heat-clearing, detoxifying, and blood-cooling effects. Although its potential in sepsis treatment has been suggested, the bioactive metabolites and underlying mechanisms remain poorly understood.Methods: Network pharmacology and molecular docking were employed to identify the therapeutic effects and mechanisms of Indirubin, the major bioactive metabolite of Isatidis Folium, in sepsis treatment. In vivo, a cecal ligation and puncture (CLP)-induced mouse sepsis model was used to evaluate the protective effects of Indirubin through histopathological analysis, ELISA, and biochemical assays. In vitro, RAW264.7 cells were stimulated with LPS and treated with varying concentrations of Indirubin. The anti-inflammatory effects of Indirubin were assessed using ELISA, apoptosis assays, and Western blotting.Results: Network pharmacology analysis identified Indirubin as the major bioactive metabolite of Isatidis Folium and EGFR and SRC as its key molecular targets. Experimental validation demonstrated that Indirubin significantly improved survival rates, alleviated tissue injury, and suppressed inflammatory responses in sepsis models. Mechanistically, Indirubin inhibited LPS-induced activation of the EGFR/SRC/PI3K and NF-κB/MAPK pathways in macrophages, significantly reducing cell death and inflammation in RAW264.7 cells.Conclusion: Indirubin, the primary bioactive metabolite of Isatidis Folium, exerts protective effects against sepsis by targeting the EGFR/SRC/PI3K and NF-κB/MAPK signaling pathways in macrophages. These findings provide a mechanistic basis for the development of Indirubin as a multi-target therapeutic agent for sepsis treatment.
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BIOMEDICINE & PHARMACOTHERAPY
·
2024
·
IF 6.9
Tingting Chen,Gaoxiang Ai,Guihong Liang,Lingfeng Zeng,Di Zhao,Jun Liu,Yaoxing Dou
Inflammatory bowel disease is linked to a higher occurrence of bone loss. Oxyberberine can effectively improve experimental inflammatory bowel disease. However, no study has shown the effect of oxyberberine on inflammatory bowel disease induced bone loss. The present study was performed to investigate the role of oxyberberine in inflammatory bowel disease induced osteoporosis in chronic inflammatory bowel disease mice model. The inflammatory bowel disease mice were orally given two doses of oxyberberine daily. Blood, colon, and bone specimens were collected for biomarker assessments and histological examinations. Bone biomechanical properties and key proteins and genes involved in the receptor activator of nuclear factor kappa-B ligand/nuclear factor kappa-B signaling pathway were evaluated. Additionally, the binding characteristics of oxyberberine and receptor activator of nuclear factor kappa-B ligand were evaluated by in silico simulation. Results indicated that oxyberberine treatment significantly attenuated the macroscopic damage, colonic shortening, and histological injury from the colon. Furthermore, oxyberberine decreased serum inflammatory cytokine levels. The intervention with oxyberberine significantly mitigated the deterioration of bone mass, biomechanical properties, and microstructural parameters. Moreover, the upregulated osteoclast formation factors in model mice were significantly abolished by oxyberberine. In silico simulation results also showed that oxyberberine was firmly bound with target protein. Hence, our findings indicated that oxyberberine had the potential to mitigate inflammatory bowel disease induced inflammation in bone, inhibit osteoclast formation through regulating the receptor activator of nuclear factor kappa-B ligand/nuclear factor kappa-B signaling pathway, and might be a valuable approach in preventing bone loss associated with inflammatory bowel disease.
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BRAIN RESEARCH BULLETIN
·
2024
·
IF 3.5
Yu Bi,Ziyi Xie,Xiang Cao,Huanyu Ni,Shengnan Xia,Xinyu Bao,Qinyue Huang,Yun Xu,Qingxiu Zhang
Microglia-associated neuroinflammation plays essential roles in pathology of acute stroke. Cedrol, a natural compound extracted from ginger, has been shown to confer inhibitory effects on inflammation in various diseases. However, whether Cedrol suppresses neuroinflammation and protects brains from acute ischemic injury still remains unclear. In this study, we found that Cedrol inhibited microglia activation and the production of inflammatory factors in LPS-challenged microglia and the penumbra region of middle cerebral artery occlusion (MCAO) mice. We also found that Cedrol reduced the infarct size and mNSS scores and improved acute cerebral ischemia-induced behavioral outcomes, suggesting remarked neuroprotection of Cedrol. Molecular docking analysis showed that Cedrol bound to estrogen receptor β (ERβ) with moderate-strong affinity. Intriguingly, treatment with fulvestrant, an ER blocker, abolished the anti-inflammatory effects of Cedrol. Cedrol significantly reversed the LPS- and MCAO-induced increases in phosphorylation levels of IκB and NF-κB P65 in primary microglia and MCAO mice, respectively. Additionally, Cedrol was observed to rescue LPS-induced shuttling of NF-κB P65 from cytoplasm to nuclei in primary microglia, indicating inhibitory effects of Cedrol on NF-κB signaling. These results suggest microglia associated neuroinflammation may be mediated by ERβ-NF-κB signaling pathway. Together, our study reveals that Cedrol protected brain function from acute cerebral ischemia through inhibition of microglia-associated neuroinflammation via ERβ-NF-κB signaling pathways, and Cedrol may serve as an alternative option for treatment of acute stroke injury.
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INFLAMMATION
·
2026
·
IF 5.4
Wang Zhengwei,Lin Jiani,Tan Guisen,Zhang Weimin,Chen Tao,Gao Ming,Liu Jiacheng,Wang Jianwei,Pan Tingzheng,Li Qingzhong,Zhang Hongtian,Shen Hongwei,He Xiaosheng,Liu Jiangang,Liu Zhuohao
The post-ischemic immune microenvironment critically balances neuroinflammation and tissue repair, making macrophage polarization a pivotal therapeutic target in cerebral infarction. Umbilical cord mesenchymal stromal cells (UCMSCs) modulate macrophage polarization primarily through paracrine signaling, while the key mediators and underlying mechanisms remain incompletely elucidated. Using proteomic array-based screening of co-culture supernatants, we identified soluble factors secreted by UCMSCs that regulate macrophage polarization. Stable soluble tumor necrosis factor receptor 1 (sTNFR1)-overexpressing (oe-sTNFR1) UCMSCs were generated via lentiviral transduction. The mechanisms by which sTNFR1 regulates macrophage polarization were investigated in vitro using immunoblotting, RT-qPCR, immunofluorescence, and flow cytometry. The therapeutic efficacy was evaluated in a rat model of middle cerebral artery occlusion (MCAO) via intracranial delivery of oe-sTNFR1 UCMSCs, with outcomes assessed via histological (Nissl and 2,3,5-triphenyltetrazolium chloride) staining, behavioral tests, and magnetic resonance imaging. To circumvent risks of genetic modification, a TNF-α-targeting nanobody (TNF-α Nb) was developed and tested in combination with wild-type UCMSCs. Proteomic analysis identified sTNFR1 as a key mediator secreted by UCMSCs for reprogramming macrophage polarization. oe-sTNFR1 UCMSCs enhanced macrophage chemotaxis and promoted reparative polarization in a paracrine-dependent manner. Mechanistically, UCMSC-derived sTNFR1 suppressed the NF-κB axis, which not only attenuated pro-inflammatory polarization but also derepressed SOCS3 signaling, thereby promoting the reparative phenotype. In MCAO rats, intracranial delivery of oe-sTNFR1 UCMSCs reshaped the post-ischemic brain microenvironment toward an anti-inflammatory and pro-repair state, improving neurological recovery through reduced infarct volume and improved functional outcomes. Furthermore, co-administration of the TNF-α Nb with wild-type UCMSCs enhanced a reparative myeloid phenotype and improved neurological outcomes compared to UCMSCs alone. This study establishes UCMSC-derived sTNFR1 as a key paracrine mediator of macrophage polarization via the sTNFR1/NF-κB/SOCS3 axis, facilitating functional recovery after ischemic stroke. The strategy combining a TNF-α Nb with UCMSCs offers a novel and clinically promising immunotherapeutic approach.
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