APPLIED CATALYSIS B-ENVIRONMENTAL
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2021
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IF 19.503
Wanqing Li,Lei Wu,Xiaochao Wu,Chuan Shi,Yongliang Li,Lei Zhang,Hongwei Mi,Qianling Zhang,Chuanxin He,Xiangzhong Ren
The precise design and controllable manufacture of electrocatalysts for efficient oxygen reactions (OER and ORR) based on the abundant elements of the earth are urgently required but challenging task. In this study, a CoS 2 /Cu 2 S heterostructured composite (CoS 2 /Cu 2 S-NF) supported by the porous carbon nanofibers is synthesized as a high-efficiency oxygen reaction electrocatalyst. As indicated from in-situ characterization methods (infrared, Raman and XRD) integrated with the density functional theory results, the heterostructures exhibited by CoS 2 and Cu 2 S could be regulated. The results show that the electron transfer/interaction between CoS 2 and Cu 2 S in the heterojunction were regulated, as well as the electronic structures of Co and Cu sites. As impacted by the structural engineering and the electronic modulation, the activity was enhanced, and the performance of electrocatalytic oxygen reactions was improved, which exhibited the lowest potential difference for (ΔE = 0.73 V) compared with commercial electrocatalysts. The liquid ZAB in accordance with on CoS 2 /Cu 2 S-NF exhibited a stable charge and discharge capacity up to 590 h and a great power density reaching 260.60 mW cm −2 . Moreover, the flexible solid-state ZAB based on CoS 2 /Cu 2 S-NF exhibited a great competitive power density (92.06 mW cm −2 ), robust flexibility and an obvious integration. As compared with single metal sulfide-NF, the Density functional theory calculations (DFT) highlight the adsorption on CoS 2 /Cu 2 S-NF side surface in the heterojunction, which more specifically demonstrates the synergistic effect in the junction. This work presents a direction for designing heterostructured junctions as electrocatalyst and moreover its great application potential in rechargeable metal-solid batteries.
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Frontiers in Pharmacology
·
2022
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IF 5.988
Lei Jin,Xiang Peng,Zeng Shengmei,Chen Le,Zhang Lei,Yuan Zhiyi,Zhang Jun,Wang Tingting,Yu Ruihong,Zhang Wanping,Ibrahim Issa Issoufou,Ma Limei,Yu Chao
Tetramethylpyrazine (TMP), a Chinese traditional herbal extraction widely used in treating cardiovascular diseases, could attenuate vascular endothelial injuries, but the underlying mechanism remains incomprehensive. Vascular glycocalyx coating on the endothelium would be damaged and caused endothelial dysfunction in the inflammatory microenvironment, which was the initial factor of morbidity of many vascular diseases, such as atherosclerosis (AS). Here, we thoroughly investigated the molecular mechanism of TMP on vascular endothelial glycocalyx in the LPS-induced inflammatory model both in vitro and in vivo. Results showed that pretreatment with TMP significantly inhibited glycocalyx degradation and monocytes adhesion to the endothelial process. Moreover, TMP pretreatment inhibited the expression of HPSE1 (a major degrading enzyme of endothelial glycocalyx), Toll-like receptor 4 (TLR4), and the translocation of nuclear factor kappa B p65 (NF-κB p65). We were utilized withTLR4 siRNA, NF-κB inhibitor, and HPSE1 overexpression analysis confirmed TMP’s protection on endothelial glycocalyx injury, which further contributed to the monocyte-endothelial adhesion process. It was indicated that TMP might suppress glycocalyx degradation through TLR4/NF-κB/HPSE1 signaling pathway. Taken together, our results enriched the occurrence molecular mechanism of glycocalyx shedding and molecular regulation mechanism of TMP in protecting integrity of the glycocalyx structure during inflammation. As TMP is currently used in clinical applications, it may be considered a novel strategy against atherosclerosis through its ability to protect endothelial glycocalyx.
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PubMed
高影响因子
CELL CYCLE
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2021
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IF 4.534
Limei Yan,Zeping He,Wei Li,Ning Liu,Song Gao
Rhophilin Rho GTPase binding protein 2 (P76RBE) belongs to rhophilin family of Rho-GTPase-binding proteins and is found to contribute to the development of diverse cancers. Data in Oncomine and Kaplan–Meier Plotter databases showed that P76RBE was upregulated in ovarian cancer tissues compared with normal tissues, and patients with high P76RBE expression had worse overall survival, which indicated P76RBE may be associated with the pathogenesis of ovarian cancer. This study aimed to investigate the role of P76RBE in ovarian cancer and to reveal the possible underlying mechanisms. The results demonstrated that P76RBE was highly expressed in ovarian cancer tissues and ovarian cancer cell lines. Functionally, silencing of P76RBE suppressed the proliferation, induced cell cycle arrest, and inhibited migration and invasion in OVCAR-3 and OV-90 cells, while overexpression of P76RBE showed opposite effects on A2780 cells. Mechanically, P76RBE silencing resulted in downregulation of integrin β1, accompanying the reduced NF-κB p65 phosphorylation and nuclear translocation. Importantly, integrin β1 knockdown effectively rescued the effects of P76RBE overexpression on ovarian cancer cells with suppressed proliferation, migration, and invasion. Additionally, in the xenograft tumors derived from OVCAR-3 and OV-90 cell lines, P76RBE knockdown inhibited tumor growth. Meanwhile, the expression of integrin β1 and NF-κB p65 phosphorylation was decreased. In summary, our findings indicate that P76RBE contributes to the progression of ovarian cancer through regulating the integrin β1/NF-κB signaling, and it may be a promising target for ovarian cancer therapy.
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IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
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2021
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IF 2.73
Jinhui Dong,Ou Xu,Jianxing Wang,Chunguang Shan,Xiumin Ren
Objective Luteolin has an anti-allergic effect but its mechanism is not clear. This study attempted to determine the mechanisms of luteolin in rhinitis.Methods Allergic rhinitis rat model was established by ovalbumin (OVA) stimulation. Then, the rats were treated with normal saline, luteolin, or lipopolysaccharide (LPS) for 14 days. Nasal symptoms were scored; the histopathological changes of nasal mucosa were detected by hematoxylin–eosin staining. Serum levels of Th1 type cytokines (IFN-γ, IL-2), Th2 type cytokines (IL-4, IL-5, IL-13), and OVA-specific IgE (sIgE) were determined by ELISA. The expressions of Toll-like receptor 4 (TLR4) and p65 in nasal mucosa were detected by Western blot or immunohistochemistry.Results Luteolin decreased symptom scores, specifically, the scores in control group, model group, model + 0.1 mg/kg luteolin, model + 1 mg/kg luteolin, and model + 10 mg/kg luteolin groups were 0.63 ± 0.52, 7.88 ± 0.83, 1.38 ± 0.52, 2.75 ± 0.46, and 5.00 ± 0.53, respectively. Luteolin ameliorated nasal mucosa inflammation by promoting the down-regulated levels of Th1 type cytokines, and suppressing the up-regulated levels of Th2 type cytokines, OVE-sIgE, TLR4, and p65. LPS further increased symptom scores, aggravated nasal mucosa inflammation, improved the unbalance of Th1/Th2 type cytokines, and lowered the expressions of OVE-sIgE, TLR4, and p65. Moreover, LPS reversed the effect of luteolin on allergic rhinitis rats.Conclusion Luteolin ameliorated inflammation and Th1/Th2 imbalance via regulating the TLR4/NF-κB pathway in allergic rhinitis rats. This study provided novel evidence that luteolin could be used as a candidate drug in allergic rhinitis treatment.
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BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
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2021
·Vol. 85
·期 7
·1665-1674
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IF 2.043
Feng Wei
This study aims to explore the effect of Tectorigenin in chronic cerebral ischemia (CCI)-induced cognitive impairment mice model. Cognitive impairment, hippocampal tissue histopathology, and myelin density in CCI mice were detected. HT22 cells were used to induce oxygen–glucose deprivation/reperfusion (OGD/R) injury. Cell viability and apoptosis of transfected HT22 cells and toll-like receptor-4 (TLR4)/nuclear factor-kappaB (NF-κB) pathway–related factor levels in hippocampal tissue and OGD/R models were detected. CCI caused cognitive impairment, hippocampal damage, and decreased myelin density in mice while promoting interleukin-1β, tumor necrosis factor-alpha, TLR4, myeloid differentiation primary response gene 88, p-p65, NLRP3, and ASC levels. Tectorigenin reversed the effects of CCI in mice and reversed the promoting effects of OGD/R on apoptosis and TLR4/NF-κB pathway–related factors levels, while overexpressed TLR4 reversed the effects of Tectorigenin in OGD/R-induced HT-22 cells. Tectorigenin alleviated cognitive impairment in CCI mice by inhibiting the TLR4/NF-κB signaling pathway.
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Applied Materials Today
·
2020
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IF 8.352
Qiongcong Xu,Liying Wang,Tong Tong,Xitai Huang,Chensong Huang,Fuxi Li,Qiao Su,Yichih Tien,Jun Wu,Wei Zhao,Xiaoyu Yin
Gallbladder cancer (GBC) is one of the most common and aggressive biliary tract diseases with limited therapeutic strategies and poor prognosis. Various therapeutic agents have been demonstrated effective in preclinical models, but high dose requirement and toxicity to normal cells limit their clinical applications. Considering the high concentration of glutathione (GSH) in GBC, we developed a GSH-responsive nanoparticle (NP) system based on biodegradable poly(disulfide amide) (Cys-8E Polymer) for targeted delivery of a BRD4 inhibitor (JQ1), which is known as a promising therapeutic agent for GBC treatment. JQ1-loaded Cys-8E nanoparticles ( [email protected] NPs) possessed a high JQ1 loading, preferable stability and redox-responsive release behavior. Additionally, the NPs showed good targeted delivery into GBC tumor spheroids and GBC patient-derived xenograft (PDX) tumors. Specifically, the intracellular GSH in tumors could trigger the release of JQ1, which induced the cell cycle arrest and apoptosis of GBC cells. RNA-sequencing analysis revealed that [email protected] NPs enhanced the effect of JQ1 through inhibiting NF-κB pathway. Importantly, [email protected] NPs significantly suppressed GBC tumor growth in the PDX model of early recurrence. No obvious systemic toxicity and organ damages were observed after treatment with [email protected] NPs. Our results demonstrate the promising therapeutic applications of [email protected] NPs for adjuvant therapy in GBC treatment.
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INFLAMMATION
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2020
·Vol. 44
·期 2
·746-757
·
IF 3.212
Gao Yang,Kang Kai,Liu Yan-song,Li Na-na,Han Qiu-yuan,Liu Hai-tao,Kong Wei-lan,Zhang Xing,Huang Rui,Yang Zhen-yu,Qi Zhi-dong,Zheng Jun-bo,Li Ming,Wang Hong-liang,Li Jia-yu,Liu Rui-jin,Wang Si-cong,Zhang Wei-hua,Zhao Ming-yan,Yu Kai-jiang
This study aimed to investigate the effect of splenectomy on dexmedetomidine-activated cholinergic anti-inflammatory pathway-mediated alleviation of LPS-induced AKI. A mouse model of septic kidney injury was established in C57BL/6 mice. A total of 30 C57BL/6 mice were randomly divided into the control group, LPS group, dexmedetomidine + LPS group, splenectomy group, splenectomy + LPS group, and splenectomy + dexmedetomidine + LPS group. The pathological effects in kidney tissues in each group were analyzed by HE staining. Apoptosis in each group was examined by the TUNEL method. Cr and Cys-C levels in each group were measured by ELISA. The expression levels of IL-6, NF-κB p65, Caspase-3, the antiapoptotic protein Bcl-2, the proapoptotic protein Bax, and α7nAChR in each group were measured by qRT-PCR and Western blotting. Dexmedetomidine alone reduced apoptosis in kidney tissue; however, apoptosis was increased after splenectomy in mice treated with dexmedetomidine. Splenectomy reduced the production of proinflammatory cytokines in circulation and had a protective effect on the kidney. Splenectomy inhibited dexmedetomidine-mediated activation of the α7nAChR pathway. Dexmedetomidine effectively alleviated LPS-induced kidney injury, and splenectomy inhibited the anti-inflammatory, antiapoptotic, and renoprotective effects of dexmedetomidine. The kidney-spleen axis is mediated by the α7nAChR-NF-κB signaling pathway and is involved in the development of AKI.
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Cancer Management and Research
·
2020
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IF 2.886
Weixu Luo,Yuanshan Han,Pan Meng,Qin Yang,Hongqing Zhao,Jia Ling,Yuhong Wang
Background Breast cancer is one of the most common cancer with high risk in females all over the world. It is usually complicated with depression, which can further accelerate the development and progression of breast tumors. We aim to identify a new drug and identify its functional mechanism in the regulation of hippocampal microglia (MG) in breast cancer complicated with depression (BCCD). Methods The activation model of MG was established by treatments from corticosterone (CORT) or lipopolysaccharides (LPS). The inhibitory effects of resatorvid on MG were investigated by CCK-8, ROS, immunofluorescence, TUNEL, scratch test, ELISA, RT-qPCR and Western blot. BCCD animal model was established using 4T1 inflammatory breast cancer cells and CORT treatment in vitro. Open field experiment (OFE), tail suspension test (TST), ELISA, RT-qPCR and Western blot experiments were utilized to examine the effects of resatorvid on the animal model in vivo. Results The cell viability and migration ability of the BCCD model group were suppressed. The expressions of inflammatory factors, ROS, and the apoptotic rate of the BCCD model group were up-regulated, in contrast to the control group. The expressions related to the TLR4/NF-κB/NLRP3 signaling in the BCCD model group were also elevated. Resatorvid reversed the above changes, which showed good therapeutic effects in depression-related behavioral changes, tumor treatment, and blood–brain barrier function. Conclusion In summary, resatorvid inhibited the activation of hippocampal MG in BCCD by regulating TLR4/NF-κB/NLRP3 signaling pathway.
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高影响因子
YONSEI MEDICAL JOURNAL
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2020
·
IF 1.914
Guang Yang,Yuan Zhao
Purpose Neonatal hypoxic ischemic encephalopathy (HIE) is an essential factor underlying neonatal death and disability. This study sought to explore the role of miR-146b-5p in regulating neonatal HIE. Materials and Methods In vitro and in vivo HIE models were established in PC12 cells and 10-day neonatal Sprague Dawley rats, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to assess miR-146b-5p expression and inflammatory factors [interleukin (IL)-6 and tumor necrosis factor (TNF)-α] in brain lesions and PC12 cells, while enzyme-linked immunosorbent assay was employed to detect the expression of oxidative stress factors (SOD and GSH-Px). Gain- and loss-assays of miR-146b-5p were conducted to verify its role in modulating the viability and apoptosis of PC12 cells under oxygen-glucose deprivation (OGD) treatment. Expression of TLR4, IRAK1, TRAF6, TAK1, and NF-κB were examined by qRT-PCR and/or Western blot. Dual luciferase activity assay was conducted to identify relationships between miR-146b-5p and IRAK1. Results In the HIE models, significant oxidative stress and inflammatory responses emerged upon upregulation of TLR4/IRAK1/TRAF6/TAK1/NF-κB signaling. Overexpression of miR-146b-5p greatly inhibited OGD-induced PC12 cell injury, inflammatory responses, and oxidative stress. Inhibiting miR-146b-5p, however, had the opposite effects. IRAK1 was found to be a target of miR-146b-5p, and miR-146b-5p overexpression suppressed the activation of IRAK1/TRAF6/TAK1/NF-κB signaling. Conclusion This study demonstrated that miR-146b-5p overexpression alleviates HIE-induced neuron injury by inhibiting the IRAK1/TRAF6/TAK1/NF-κB pathway.
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高影响因子
CHEMOSPHERE
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2020
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IF 5.778
Chao Fang,Tian Ou,Xingyu Wang,Min Rui,Wenhai Chu
Ultrafiltration (UF), nanofiltration (NF) and reverse osmosis (RO) are widely used in drinking water treatment and wastewater recycling. However, limited information was available regarding their performance in removing trihalomethanes (THMs). The present study investigated the effect of feed solution characteristics and membrane fouling on THM removal by UF/NF/RO membranes. The results indicated that THMs were poorly removed by UF membrane, and the removal was dominated by hydrophobic adsorption. In contrast, high removal of THMs was observed for NF/RO membranes, which was contributed by both size exclusion and hydrophobic adsorption. By comparing the adsorption of THMs on NF/RO membranes at different feed concentration, it was found that the role of hydrophobic adsorption was more important at lower feed concentration. The removal of THMs by UF/NF/RO membranes increased with increasing feed concentration, which can be ascribed to the enhanced diffusion at higher concentration gradient. With increasing ionic strength, THM removal was decreased significantly for UF membrane, but the removal by NF/RO membranes remained largely unchanged. By comparing THM removal by clean and fouled membranes, the effect of membrane fouling was examined. The removal of most THMs (except trichloromethane) decreased after fouling for UF membrane, whereas decreased removal was only observed for iodinated THMs for fouled NF/RO membranes.
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JOURNAL OF INDUSTRIAL AND ENGINEERING CHEMISTRY
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2022
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IF 6.76
Jianzhi Wang,Yu Luo,Tong Xu,Ziyi Guo,Guopeng Chen,Yuchen Ren,Yanan Xue,Ning Cai,Hui Li,Faquan Yu
The development of low-cost and highly efficient electrocatalysts for oxygen evolution reaction (OER) with good conductivity, high specific surface area and abundant oxygen vacancies is of great significance for the future renewable energy conversion and storage system. Herein, Ag doped NiMoO 4 materials on the Ni foam (NiMoO 4 /Ag/NF) with rich oxygen vacancies were successfully prepared by hydrothermal strategy and layer by layer assembly method. The Ag ions are doped in-situ to promote electron transfer and compensate for the poor conductivity of metal oxides. The suitable air annealing treatment is used to create rich oxygen vacancies. The high specific surface area and one-dimensional characteristics of the cross mesoporous nanorod skeleton are responsible for the increased exposure of active centers and the rapid charge transfer behavior. The NiMoO 4 /Ag/NF exhibits high activity for OER in alkaline solution (an overpotential of 275 mV at the current density of 20 mA cm −2 ) and low Tafel slope (53.67 mV dec −1 ), and a satisfying durability in 1.0 M KOH. This study provides an effective method for the preparation of Ag doped one-dimensional nanomaterials with excellent OER catalytic performance and electrochemical stability.
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npj Science of Food
·
2026
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IF 9.7
Jin Hongchen,Bai Huasong,Liu Tong,Wang Hengyan,Yin Yulong,Ruan Siyu,Li Yunliang,Wang Zhanzhong
Anti-aging bioproducts from natural active ingredients represent a core future direction in food research. Cardiovascular aging drives most age-related disorders. This study investigated the anti-aging effects of a postbiotic preparations derived from brown algae extract fermented by Bifidobacterium adolescentis Life Age 20 (LA20FM). Multi-model were used, including doxorubicin (DOX)-induced senescent canine (CVECs) and feline vascular endothelial cells (FVECs), senescence-accelerated mouse prone 8 (SAMP8) mice, Caenorhabditis elegans , and naturally aged dogs and cats. In vitro, LA20FM markedly attenuated DOX-induced endothelial senescence, reduced the secretion of senescence-associated secretory phenotype factors, and restored endothelial function-related markers. In aged SAMP8 mice, LA20FM alleviated vascular remodeling, reduced circulating senescence- and inflammation-related biomarkers, and improved physiological performance. In C. elegans , LA20FM extended lifespan by approximately 30%, enhanced reproductive capacity, and significantly reduced intracellular reactive oxygen species levels. Comparable improvements in physiological parameters were also observed in aged dogs and cats. Transcriptomic analyses of CVECs and SAMP8 vascular tissues revealed that LA20FM treatment was accompanied by downregulation of NF-κB-related inflammatory signaling. Phorbol 12-myristate 13-acetate rescue experiments and early time-point analyses further supported NF-κB signaling as an early and functionally important mediator of its protective effects. Metabolomic analysis further revealed metabolic remodeling characterized by reduced lipid-associated metabolic activity and enhanced amino acid biosynthesis and antioxidant-related metabolism. Collectively, these findings indicate that LA20FM alleviates canine and feline vascular endothelial senescence and improves aging-associated phenotypes across multiple experimental models, supporting its potential as a postbiotic preparation for canine and feline nutritional intervention against vascular functional decline and further aging.
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