JOURNAL OF SURGICAL RESEARCH
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2022
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IF 2.417
Ming Deng,Ping Xie,Junqi Liu,Yan Zhou,Zhonghui Chen,Yonggang Ma,Jianwei Yang
Introduction α-Cyperone has anti-inflammatory activities, but its effects on spinal cord injury (SCI) remain obscure. Thus, this study attempts to investigate the effects and modulatory mechanisms of α-Cyperone on SCI. Materials and methods An SCI model was established in rats which were further treated with α-Cyperone. Basso-Beattie-Bresnahan (BBB) scoring was used to assess motor rehabilitation of rats modeled with SCI. The spinal cord tissues were collected, and the effect of α-Cyperone on the histopathology of rats modeled with SCI was detected by hematoxylin-eosin staining. Rat primary cortical neuron was stimulated with H 2 O 2 and further treated with α-Cyperone and nuclear factor erythroid 2-related factor 2 (Nrf2) inhibitor ML385. The levels of Nrf2, interleukin-6 (IL-6), nuclear factor kappa B (NF-κB), Akt, toll-like receptor 4 (TLR4), and tumor necrosis factor-alpha (TNF-α) were detected by immunofluorescence staining and western blotting . Results α-Cyperone elevated the BBB score and ameliorated the damage of spinal cord tissue in rats modeled with SCI. The levels of IL-6, Nrf2, NF-κB, TLR4, and TNF-α were upregulated, whereas that of Akt was downregulated in rats and cells modeled with SCI. Furthermore, α-Cyperone diminished the levels of IL-6, NF-κB, TLR4, and TNF-α, while augmenting those of Nrf2 and Akt in rats and cells modeled with SCI. ML385 inhibited the Nrf2 level that had been promoted by α-Cyperone in the nucleus and elevated the Nrf2 level that had been suppressed by α-Cyperone in the cytosol of cells modeled with SCI. ML385 increased the levels of IL-6, NF-κB, TLR4, and TNF-α that had been inhibited by α-Cyperone and decreased the Akt level that had been enhanced by α-Cyperone in cells modeled with SCI. Conclusions α-Cyperone suppressed SCI-induced inflammation and spinal cord tissue damage via activating Akt/Nrf2 and suppressing NF-κB pathways.
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Frontiers in Pharmacology
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2022
·
IF 5.988
Chai Yuhui,Cai Yawen,Fu Yu,Wang Yingdi,Zhang Yiming,Zhang Xue,Zhu Lingpeng,Miao Mingxing,Yan Tianhua
Depression is a common and serious mental disorder. Data on its pathogenesis remain unclear and the options of drug treatments are limited. Here, we explored the role of pyroptosis, a novel pro-inflammatory programmed cell death process, in depression as well as the anti-depression effects and mechanisms of salidroside (Sal), a bioactive extract from Rhodiola rosea L. We established a corticosterone (CORT)-induced or lipopolysaccharide (LPS)-induced mice in vivo, and CORT, or nigericin (NLRP3 agonist)-induced PC12 cells in vitro. Our findings demonstrated that Sal profoundly mediated CORT or LPS-induced depressive behavior and improved synaptic plasticity by upregulating the expression of brain-derived neurotrophic factor (BDNF) gene. The data showed upregulation of proteins associated with NLRP3-mediated pyroptosis, including NLRP3, cleaved Caspase-1, IL-1β, IL-18, and cleaved GSDMD. The molecular docking simulation predicted that Sal would interact with P2X7 of the P2X7/NF-κB/NLRP3 signaling pathway. In addition, our findings showed that the NLRP3-mediated pyroptosis was regulated by P2X7/NF-κB/NLRP3 signaling pathway. Interestingly, Sal was shown to ameliorate depression via suppression of the P2X7/NF-κB/NLRP3 mediated pyroptosis, and rescued nigericin-induced pyroptosis in the PC12 cells. Besides, knock down of the NLRP3 gene by siRNA markedly increased the inhibitory effects of Sal on pyroptosis and proinflammatory responses. Taken together, our findings demonstrated that pyroptosis plays a crucial role in depression, and Sal ameliorates depression by suppressing the P2X7/NF-κB/NLRP3-mediated pyroptosis. Thus, our study provides new insights into the potential treatment options for depression.
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IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
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2022
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IF 3.712
Haihua Zhang,Wuying Lang,Sufen Li,Chao Xu,Xiumin Wang,Yunyu Li,Zhiqiang Zhang,Tonglei Wu,Minshan Feng
Objective Corynoline is an active substance extracted from Corydalis bungeana Turcz and exerts a therapeutic effect in multiple diseases by alleviating inflammatory response. The present study sought to elucidate the role of corynoline in ulcerative colitis (UC).Methods The experimental colitis models were induced in BALB/c mice via receiving a drinking water supplemented with 3.5% (I) dextran sulfate sodium (DSS) ad libitum for 7 days.Results Corynoline administration inhibited body weight loss, colon shortening, disease activity index and colonic pathomorphological changes in DSS-treated mice. Besides, corynoline down-regulated the levels of pro-inflammatory interleukin (IL)-1β, IL-6 and tumor necrosis factor Alpha (TNF-α), as well as decreased myeloperoxidase (MPO) activity in the colon of DSS-treated mice. In addition, severe oxidative stress in the colonic tissues of DSS-treated was mitigated by corynoline treatment. However, these beneficial effects were reversed by a specific nuclear factor E2-related factor 2 (Nrf2) inhibitor ML385 intervention. Further evidence confirmed that corynoline promoted Nrf2 nuclear migration and heme oxygenase-1 gene expression in the colonic tissues of UC mice. Besides, corynoline treatment restrained colonic nuclear factor-kappa B (NF-κB) activation as proved by the decrease in phosphorylation and nuclear translocation of NF-κB.Conclusions Corynoline ameliorates DSS-induced mouse colitis, which may provide a promising therapeutic strategy for UC treatment.
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Nanomaterials
·
2022
·Vol. 12
·期 15
·2640
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IF 5.719
Liming Yang,Tao Yang,Yafeng Chen,Yapeng Zheng,Enhui Wang,Zhentao Du,Kuo-Chih Chou,Xinmei Hou
The development of bifunctional electrocatalysts with efficient oxygen evolution reaction (OER) and hydrogen evolution reaction (HER) is still a key challenge at the current stage. Herein, FeNi LDH/V2CTx/nickel foam (NF) self-supported bifunctional electrode was prepared via deposition of FeNi LDH on V2CTx/NF substrate by hydrothermal method. Strong interfacial interaction between V2CTx/NF and FeNi LDH effectively prevented the aggregation of FeNi LDH, thus exposing more catalytic active sites, which improved electrical conductivity of the nanohybrids and structural stability. The results indicated that the prepared FeNi LDH/V2CTx/NF required 222 mV and 151 mV overpotential for OER and HER in 1 M KOH to provide 10 mA cm−2, respectively. Besides, the FeNi LDH/V2CTx/NF electrocatalysts were applied to overall water splitting, which achieved a current density of 10 mA cm−2at 1.74 V. This work provides ideas for improving the electrocatalytic performance of electrocatalysts through simple synthesis strategies, structural adjustment, use of conductive substrates and formation of hierarchical structures.Keywords:V2CTxMXene;layered double hydroxide;nanohybrids;overall water splitting
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MOLECULAR MEDICINE
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2022
·Vol. 28
·期 1
·1-20
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IF 6.376
Ming Shaoxiong,Tian Jia,Ma Ke,Pei Chengbin,Li Ling,Wang Zeyu,Fang Ziyu,Liu Min,Dong Hao,Li Weijian,Zeng Jianwen,Peng Yonghan,Gao Xiaofeng
Background Kidney stones are composed of approximately 70–80% calcium oxalate. However, the exact mechanism of formation of calcium oxalate kidney stones remains unclear. In this study, we investigated the roles of endoplasmic reticulum stress (ERS), reactive oxygen species (ROS), and the NF-κB signalling pathway in the pathogenesis of oxalate-induced renal tubular epithelial cell injury and its possible molecular mechanisms. Methods We established a model to evaluate the formation of kidney stones by intraperitoneal injection of glyoxylic acid solution into mice and assessed cell morphology, apoptosis, and the expression levels of ERS, ROS, and NF-κB signalling pathway-related proteins in mouse renal tissues. Next, we treated HK-2 cells with potassium oxalate to construct a renal tubular epithelial cell injury model. We detected the changes in autophagy, apoptosis, and mitochondrial membrane potential and investigated the ultrastructure of the cells by transmission electron microscopy. Western blotting revealed the expression levels of apoptosis and autophagy proteins; mitochondrial structural and functional proteins; and ERS, ROS, and NF-κB (p65) proteins. Lastly, we studied the downregulation of NF-κB activity in HK-2 cells by lentivirus interference and confirmed the interaction between the NF-κB signalling and ERS/ROS pathways. Results We observed swelling of renal tissues, increased apoptosis of renal tubular epithelial cells, and activation of the ERS, ROS, and NF-κB signalling pathways in the oxalate group. We found that oxalate induced autophagy, apoptosis, and mitochondrial damage in HK-2 cells and activated the ERS/ROS/NF-κB pathways. Interestingly, when the NF-κB signalling pathway was inhibited, the ERS/ROS pathway was also inhibited. Conclusion Oxalate induces HK-2 cell injury through the interaction between the NF-κB signalling and ERS/ROS pathways.
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ORAL DISEASES
·
2022
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IF 4.068
Minmin Sun,Yaoting Ji,Shuhui Zhou,Rourong Chen,Hantao Yao,Minquan Du
Objective The objective of the study was to determine the anti-osteoclastogenic potential of ginsenoside Rb3 for the treatment of periodontitis. Methods The anti-osteoclastogenic effect was determined using RANKL-induced RAW264.7 cells and murine bone marrow-derived macrophages followed by TRAP and phalloidin staining. Expression of osteoclastogenesis-related genes and proteins were examined by qPCR and WB. Activation of signaling pathways was detected by WB and IHC techniques. Experimental periodontitis rat model was built up by gingival injections of P. gingivalis LPS. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT, IHC, H&E, and TRAP staining analyses. Results Rb3 dramatically inhibits RANKL-induced osteoclastogenesis. Nfatc1, Mmp9, Ctsk, Acp5 mRNA, and MMP9, CTSK proteins were dose-dependently downregulated by Rb3 pretreatment. WB results revealed that Rb3 suppressed activations of p38 MAPK, ERK, and p65 NF-κB, and the inhibition of ERK was most pronounced. Consistently, IHC analysis revealed that p-ERK was highly expressed in alveolar bone surface, blood vessels, odontoblasts, and gingival epithelia, which were notably suppressed by Rb3 treatment. H&E staining and micro-CT analyses showed that Rb3 significantly attenuated gingivitis and alveolar bone resorption in rats. Conclusion Rb3 inhibits RANKL-induced osteoclastogenesis and attenuates P. gingivalis LPS-induced gingivitis and alveolar bone resorption in rats via ERK/NF-κB signaling pathway.
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JOURNAL OF MEMBRANE SCIENCE
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2021
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IF 8.742
Jiayu Tian,Bin Song,Shanshan Gao,Bart Van der Bruggen,Ruijun Zhang
It is a grand challenge to achieve the omnifarious performance promotion of the thin film composite (TFC) nanofiltration (NF) membranes due to the mutual influence among membrane permeability, selectivity and antifouling ability. Hereon, a rational strategy denoted as hyperbranched polyester (HPE) intervened interfacial polymerization (IP) was proposed to simultaneously improve various membrane properties. HPE with special molecular structure was mixed into the piperazine (PIP) solution to form a composite aqueous phase, and then a modified selective layer was generated via the IP reaction with the trimesoyl chloride (TMC). In this process, the diffusion rate of PIP monomer was reduced because of the steric hindrance effect brought by HPE and the hydrogen bonding interaction between PIP and HPE. Meanwhile, the primary hydroxyl groups in HPE also participated in the polymerization reaction. The structure and separation performance of the resultant membranes were systematically investigated. The results showed that when the HPE dosage was 1 w/v%, the thickness of the modified selective layer was as low as 8.34 nm. The pure water permeability of the corresponding TFC NF membrane was high to 50.62 L·m-2·h-1·bar-1, while keeping the Na2SO4 rejection over 98%. Moreover, this membrane presented long-term stability and antifouling performance.
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JOURNAL OF MEMBRANE SCIENCE
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2021
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IF 8.742
Yue Zong,Ruijun Zhang,Shanshan Gao,Hailin Chang,Bart Van der Bruggen,Jiayu Tian
A fatal problem faced by conventional nanofiltration (NF) membranes is that they cannot be dry-stored without protective agent. Hereon, an anti-drying NF membrane is successfully constructed on a PTFE microfiltration (MF) substrate. It is demonstrated that the selection of PTFE MF substrate is the key factor for ensuring the desiccation tolerance. Meanwhile, a novel interfacial polymerization strategy denotes (one and a half)-step interfacial polymerization (3/2-IP) makes it possible to construct a defect-free polyamide film on the PTFE substrate. During the 3/2-IP process, IP reaction is doubly proceeded only by soaking piperazine (PIP) solution once and trimesoyl chloride (TMC) solution twice, because PIP droplets will be reproduced on membrane surface due to the interfacial tension, vapor condensation and gas driven during heat-treatment. The first IP reduces the substrate pore size and improves its hydrophilicity. Then an intact polyamide film with nano-wrinkled structure is produced in the second IP reaction. Our findings provide a valuable route for fabricating thin-film composite (TFC) NF membranes with desiccation tolerance and desirable separation performance.
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Journal of Energy Chemistry
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2021
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IF 9.676
Guojuan Hai,Jianfeng Huang,Liyun Cao,Koji Kajiyoshi,Long Wang,Liangliang Feng,Jun Chen
The electrochemical conversion is closely correlated with the electrocatalytic activities of the electrocatalyst. Herein, the urchin-like Ni-doped W 18 O 49 /NF with enriched active sites was prepared by solvothermal method followed by a low-temperature pyrolysis treatment was reported. Results demonstrate that the incorporation of Ni-doping triggers the lattice distortion of W 18 O 49 for the increasement of oxygen defects. Further, high-valent W 6+ are partially reduced to low-valent W 4+ , wherein the electrons originate from the oxidation process of Ni 2+ to Ni 3+ . The Ni 3+ ions show an enhanced orbital overlap with the OER reaction intermediates. The generated W 4+ ions contribute to release oxygen vacancies, eventually reorganizing Ni-doped W 18 O 49 /NF to unique electrochemical active species with a special amorphous-crystalline interface (AM/NiWO x /NiOOH/NF). Simultaneously, the reconstruction results in an optimized valence band and conduction band. Eventually, the resultant AM/NiWO x /NiOOH/NF with abundant active sites and improved oxidation/reduction capability exhibits more superior catalytic performance compared with the Ni-doped W 18 O 49 /NF counterpart. This study gives more insights in the electrochemical evolution of the tungsten-based oxide and provides effective strategies for optimizing the catalytic activity of materials with inherent hydrogen evolution reaction limitations.
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APPLIED SURFACE SCIENCE
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2021
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IF 6.707
Guojuan Hai,Jianfeng Huang,Liyun Cao,Koji Kajiyoshi,Long Wang,Liangliang Feng
Designing and synthesizing heterojunction electrocatalyst with abundant active sites is critical to optimize the activity of electrochemical water splitting. Herein, a typical hierarchical W 18 O 49 /NiWO 4 heterojunction grown on nickel foam was successfully synthesized via a multistep synthesis strategy. The electrochemical oxidation and reduction process triggers the amorphization of W 18 O 49 and significantly enhances the interfacial interaction, thereby endowing the composites with enriched active sites. The W 18 O 49 /NiWO 4 /NF is completely reconstructed to NiWO 4 /NF and NiWO 4 /NiOOH/NF with amorphous-crystalline interface (denoted as H-AM/NiWO 4 /NF for HER and O-AM/NiWO 4 /NiOOH/NF for OER). The valence of tungsten ions is well modulated to achieve a high proportion of tetravalent W (IV) active sites accompanied by abundant oxygen vacancies. The increased Ni (III) ions as OER active sites have strong orbital overlap with reaction intermediate, which stabilize the low-valent W (IV) by producing more NiOOH species during the oxygen evolution reaction. Benefiting from the amorphous–crystalline composites, unsaturated W (IV) sites, abundant oxygen vacancies, and highly active NiOOH species, the activated electrocatalyst exhibits excellent electrocatalytic activity, achieving a small overpotential of 1.53 V at 10 mA·cm −2 for water-splitting and maintaining long-term stability at least 100 h.
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FASEB JOURNAL
·
2021
·Vol. 35
·期 7
·e21497
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IF 5.192
Sha Tu,Yanzhi Jiang,Haihua Cheng,Xiangning Yuan,Ying He,Yu Peng,Xiongqun Peng,Zhangzhe Peng,Lijian Tao,Huixiang Yang
Despite the increasing understanding of the pathophysiology of hepatic fibrosis, the therapies to combat it remain inadequate. Fluorofenidone (AKF-PD) is a novel pyridone agent able to ameliorate hepatic fibrosis in an experimental hepatic fibrosis model induced by dimethylnitrosamine. However, the underlying mechanism remains to be further elucidated. In light of the critical role of the NF-κB pathway in inflammation and hepatic fibrosis, together with the preliminary finding that AKF-PD decreases the release of proinflammatory cytokines in the endotoxemia and unilateral ureteral occlusion model, the aim of this study was to explore whether AKF-PD exerts an antifibrotic effect in hepatic fibrosis by inhibiting inflammation and suppressing the activation of the NF-κB pathway in vivo and in vitro. To test this possibility, the effect of AKF-PD on hepatic fibrosis models induced by both carbon tetrachloride (CCL 4 ) and porcine serum (PS) was investigated. Our results showed that AKF-PD treatment ameliorated hepatic injury and fibrosis in both models. Furthermore, the administration of AKF-PD induced a robust anti-inflammatory reaction revealed by the downregulation of the proinflammatory cytokines as well as the suppression of the infiltration of inflammatory cells in the fibrotic liver. The analysis of the mechanism of action demonstrated that the attenuation of the production of proinflammatory cytokines and chemokines mediated by AKF-PD in vivo and in vitro were accompanied by the suppression in the activation of the NF-κB signaling pathway. In conclusion, AKF-PD might be considered as an antifibrotic agent attenuating hepatic inflammation and fibrosis potentially through the suppression of the NF-κB pathway.
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Archives of Medical Science
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2020
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IF 2.807
Ning Xu,Lili Wang,Shiping Fu,Bin Jiang
Introduction Osteosarcoma is the most common primary malignancy of the bone. The existing adjuvant chemotherapy regimens, while improving the overall survival, have been limited by the significant systemic toxicity. Substantial clinical and research efforts are being invested to develop novel pharmaceutical agents. Resveratrol (Res) has been suggested to have a chemopreventive effect. However, the mechanism of Res in osteosarcoma remains to be elucidated. Material and methods The MG-63 osteosarcoma cell culture model was used to investigate the chemotherapeutic effect of Res. MTT assay, wound healing assay, and Transwell migration assay were used to document the effect of Res on cell proliferation, migration, and invasion, respectively. Apoptosis in MG-63 cells was quantified with the TUNEL assay. Western blotting analysis was used to examine the molecular changes following Res treatment. Data processing and analysis were conducted using GraphPad Prism 5.0. P < 0.05 was considered statistically significant. Results Our data suggested that Res blocks cell proliferation, migration, and invasion, and activates apoptotic cell death in osteosarcoma MG-63 cells. We found that Res potentially down-regulates nuclear factor κB (NF-κB) and Akt intracellular signaling transduction. Moreover, the combination of Res and pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor, resulted in synergistic growth inhibition of osteosarcoma. Conclusions Our in vitro preclinical study in the MG-63 cell line model supports the translation of Res to the clinical management of patients with osteosarcoma.
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