JOURNAL OF ALLOYS AND COMPOUNDS
·
2022
·
IF 6.371
Rui Yao,Leran Liu,Jinwei Wang,Yun Wu,Qiang Zhao,Jinping Li,Guang Liu
Electrochemical water splitting is a vital means of producing hydrogen in the future. However, the sluggish kinetics of the oxygen evolution reaction (OER) at the anode of the water electrolysis limits its efficiency. Moreover, high current density (≥500 mA/cm 2 ) hydrogen production that meets industrial requirements and remains relatively stability is the trend currently. Herein, we reported a three-dimensional porous nanosheets array electrocatalyst FeVO 4 /NF-a synthesized by electrochemical activation and hydrothermal method . The developed FeVO 4 /NF-a electrode represents excellent OER performance at high current densities, which allows a low overpotential of 376 mV to achieve 1000 mA/cm 2 and keeps its durability for 50 h. Structural characterizations and electrochemical analyses show that the NF surface was converted to the active phase NiOOH for OER during electrochemical activation. The introduction of Fe 3+ and V 3+ changes the electron distribution of elements on the catalyst surface and optimizes its intrinsic activity. Additionally, the three-dimensional network structure of FeVO 4 /NF-a facilitates the gas diffusion and the contact between the catalyst with the electrolyte. This work will provide new ideas for hydrogen production from water electrolysis toward high current density.
研究领域:
材料科学
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电化学
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产品关联
DOI
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2022
·
IF 5.895
Sen Li,Yu Chen,Yu Zhang,Hongyan Lv,Lei Luo,Shuo Wang,Xiao Guan
Coffee cherry husks, the main byproduct of coffee production, contain an abundance of polyphenols. In this study, dextran sodium sulfate (DSS)-induced colitis mice were used to study the protective effects of polyphenolic extracts of coffee cherry husks (CCHP) on inflammation. The results indicated that CCHP administration alleviated the histological changes of DSS-induced colitis in mice and downregulated the mRNA level of TNF-α, IL-1β, IL-6 and Cox-2. Interestingly, CCHP inhibited the activation of microglia and suppressed neural inflammation in the brain. The TLR4/Myd88/NF-κB signaling pathway was examined and found to be inhibited by CCHP. Furthermore, a determination of the gut microbiota showed that an alteration of microbiota induced by DSS was restored by CCHP, including the decrease of the relative abundance of Proteobacteria and the increase of Bacteroidota. In conclusion, our results revealed the great potential of CCHP to alleviate brain inflammation in colitis mice by inhibiting the NF-κB signaling pathway and regulating gut microbiota.
研究领域:
药理学
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免疫学
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神经科学
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微生物学
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产品关联
DOI
PubMed
高影响因子
Cell Communication and Signaling
·
2025
·Vol. 23
·期 1
·1-17
·
IF 8.9
Xu Teng,Wang Yaning,Zhao Zechen,Wang Jinsong,Zhao Zhenyuan,Yang Yuemei,Song Xiaomeng,Lai Qingguo
Background Tumor dissemination is a life-threatening event which confers to most cancer-related deaths with limited effective therapeutic option. TNFα-induced protein 2 (TNFAIP2) reveals pro-metastasis potential in several cancers. However, its definite role and underlying mechanism in oral squamous cell carcinoma (OSCC) is largely unknown. Methods The impact of TNFAIP2 on tumor metastasis was assessed based on the conditional knockout mouse with 4-nitroquinoline-1-oxide (4NQO) induced OSCC model through feature and immunohistochemistry analysis. To explore the specific mechanism, enrichment analysis and co-immunoprecipitation were applied. Meanwhile, the nano-hydroxyapatite (nHAp) and poly-L-lysine (PLL) based RNA interference delivery system was designed to restrict tumor dissemination. Results The conditional knockout Tnfaip2 in epithelium reduced tumor initiation rate, differentiation degree and cervical lymph node metastasis (LNM) in mouse exposed to 4NQO. Enrichment analysis suggested nuclear factor-kappa B (NF-κB) signaling was associated with these effects. Western blot proved that TNFAIP2 prevented the ubiquitin proteasome degradation of inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta (IKKβ), a classical transcriptional activator protein in NF-κB signaling. Mechanistically, TNFAIP2 was demonstrated to competitively interact with kelch-like ECH-associated protein 1 (KEAP1) to avoid IKKβ from ubiquitination at K63 and proteasomal degradation subsequently, which finally sustained NF-κB signaling and facilitated tumor metastasis by enhancing epithelial-mesenchymal transition (EMT) and lymphangiogenesis. Notably, the synthetic small interfering RNA delivery systems nHAp@PLL-siTnfaip2 showed significant effect in attenuating tumor progression of OSCC mouse. Conclusion Above results showed TNFAIP2 promoted EMT and lymphangiogenesis of OSCC by regulating NF-κB signaling, a mechanism that was dependent on the interaction with KEAP1 competitively. The nHAp based TNFAIP2 interference might serve as a novel therapeutic in limiting OSCC metastasis.
研究领域:
肿瘤学
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分子生物学
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口腔医学
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生物化学
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产品关联
DOI
PubMed
高影响因子
IONICS
·
2022
·Vol. 28
·期 8
·3935-3944
·
IF 2.961
Wu Yanxia,Chen Xiangping,Su Lirong,Wang Qingtao,Ren Shufang
Increasing active sites by constructing a heterostructure is a very effective method to improve the electrocatalytic performance. In this work, we synthesized a three-dimensional self-supporting Ni 2 P-Ni 12 P 5 /NF heterostructure supported on nickel foams by hydrothermal reaction and low-temperature phosphorization, used as an efficient hydrogen evolution reaction (HER) electrocatalyst. The structure, composition, morphology, and HER performance of the catalyst were characterized by XRD, XPS, SEM, TEM, and electrochemical workstation. The experimental results show that the Ni 2 P-Ni 12 P 5 /NF heterostructure demonstrates better HER catalytic activity in 0.5 M H 2 SO 4 , only requiring an overpotential of 124 mV at 10 mA cm −2 with a Tafel slope of 84.1 mV dec −1 and displaying good long-term stability. The high activity and stability of the as-synthesized Ni 2 P-Ni 12 P 5 /NF catalyst in HER are mainly due to the synergy between Ni 2 P-Ni 12 P 5 with a unique heterostructure and nickel foam conductive substrate with a three-dimensional porous structure, which is beneficial to increase the electrocatalytic active area and thus provide more active sites.
研究领域:
材料科学
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电化学
✓ 已验证
DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2022
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IF 5.714
Haihua Zhang,Jing Wang,Wuying Lang,Hongli Liu,Zhiqiang Zhang,Tonglei Wu,Hongqiang Li,Liya Bai,Qiumei Shi
Methotrexate (MTX) treats various diseases but also damages intestinal barrier and leads to enteritis. Albiflorin (ALB) has a variety of pharmacological effects, including antioxidant, anti-inflammation and anti-apoptosis. In the present study, we evaluated the therapeutic effect of ALB on MTX-induced enteritis and investigated the possible mechanisms involved. Male SD rats were intraperitoneally injected with 7 mg/kg MTX for three consecutive days to establish the enteritis model. ALB (20 or 40 mg/kg/day) was intragastrically administrated since two days prior MTX treatment and lasted for six days. We found that ALB treatment increased body weight and intestinal weight of rats with MTX injection. The disease activity index (DAI) score was also decreased after ALB administration. In histological examination, ALB treatment attenuated inflammatory cells infiltration and promoted survival of goblet cells. In detection of inflammatory-associated factors, ALB treatment decreased CD68 + cells infiltration, inhibited myeloperoxidase activity, and suppressed intercellular cell adhesion molecule-1 and cyclooxygenase-2 expression. Additionally, ALB reduced malondialdehyde, glutathione levels, inhibited superoxide dismutase activity and suppressed reactive oxygen species production. Moreover, ALB treatment effectively inhibited NLRP3, as well as caspase 1 p20 and interleukin (IL)-1β and 18 expression. Finally, nuclear factor-κB (NF-κB) p65 phosphorylation and nuclear translocation were also demonstrated to be blocked upon ALB treatment. In conclusion, our findings indicated that ALB alleviated MTX-induced enteritis via inhibiting the NF-κB/NLRP3 pathway.
研究领域:
药理学
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免疫学
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胃肠病学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF COLLOID AND INTERFACE SCIENCE
·
2023
·
IF 9.9
Yucheng Dong,Xichun Zhang,Xuyun Wang,Fangfang Liu,Jianwei Ren,Hui Wang,Rongfang Wang
The development of efficient electrocatalysts for large-scale water electrolysis is crucial and challenging. Research efforts towards interface engineering and electronic structure modulation can be leveraged to enhance the electrochemical performance of the developed catalysts. In this work, a surface-engineered Co-Ni 3 N/NF heterostructure electrode was prepared based on Kirkendall effect for high-current water electrolysis. In the experiments, the textural feature and intrinsic activity of the Co-Ni 3 N/NF heterostructure were tuned through cobalt-doping and the creation of structural defects. As a result, the increased surface energy endowed Co-Ni 3 N/NF heterostructure with superhydrophilic and superaerophobic properties. Meanwhile, the contact area of the gas–liquid-solid three phases was optimized. With a large underwater bubble contact angle (CA) of 169°, the electrolyte solution can infiltrate the Co-Ni 3 N/NF electrode within 150 ms. Sequentially, the generated gas bubbles were able to detach at high frequency, which ensured the rapid mass exchange. The performance tests showed that the optimal Co-Ni 3 N/NF electrode sample reached current densities of 100 mA cm −2 and 500 mA cm −2 at the overpotentials of 98 mV and 123 mV, respectively. Benefiting from the reduction of hydrogen embrittlement, the HER performance of the prepared Co-Ni 3 N/NF electrode sample decreased slightly after 100 h durability test, but the overall structure remained well. Those results allowed us to conclude that the prepared Co-Ni 3 N/NF electrocatalyst holds the promises for large-scale water electrolysis in industries. More specifically, this work provided a new perspective that the efficiency of electrocatalysts for large-scale water electrolysis can be enhanced by constructing a heterostructure with good wettability and gas repellency.
研究领域:
材料科学
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电化学
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能源催化
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产品关联
DOI
PubMed
高影响因子
Discover Oncology
·
2023
·Vol. 14
·期 1
·1-14
·
IF 2.2
Yu Zhong,Ouyang Ling
Background Odd-skipped related 1 (OSR1) has been reported as a tumor suppressor gene in various malignant tumors. The mechanism through which OSR1 regulates ovarian cancer (OC) progression remains unclear. Materials and methods Immunohistochemistry was utilized to evaluate OSR1 expression in patients with ovarian cancer. We investigated the association between clinicopathological parameters and OSR1 expression in OC patients and the influence of OSR1 expression on patient survival and prognosis. OC cells with OSR1 overexpression or knockdown were established and validated using Western blot and Quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The influence of OSR1 on the NF-κB pathway was examined by analyzing the p-IκBα, IκBα, p65, and p-p65 protein expression. In vitro assays, such as cell cycle assay, Cell Counting Kit-8 (CCK-8), transwell invasion assay, wound healing migration assay, enzyme-linked immunoassay (ELISA), and Annexin V/PI flow cytometry apoptosis assay, were conducted to explore the effect of OSR1 knockdown or dual inhibition of OSR1 and the NF-κB pathway on OC malignant biological behavior. Results OSR1 expression was downregulated in OC tissues, with significant associations observed between its expression and The International Federation of Gynecology and Obstetrics (FIGO) stage and tissue differentiation. Low OSR1 expression in OC patients correlated with reduced overall survival (OS) rates and poor prognosis . In vitro , experiments confirmed a negative correlation between OSR1 expression and NF-κB pathway activity. OSR1 knockdown facilitated OC cell malignant biological behavior, while the NF-κB pathway inhibitor (Bay 11-0782) reversed the impacts of OSR1 knockdown on cell proliferation, migration, invasion, and apoptosis. Conclusion Our findings indicate that OSR1 is downregulated and associated with OC prognosis. OSR1 suppresses NF-κB pathway activity and inhibits OC progression by targeting the NF-κB pathway.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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癌症研究
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产品关联
DOI
PubMed
高影响因子
INORGANIC CHEMISTRY COMMUNICATIONS
·
2025
·
IF 5.4
Xiaoyu Qiu,Linting Zou,Jianmei Cen,Xingnian Duan
In this research, Mo-oxides complexes combined with Co(OH) 2 grown on three-dimensional (3D) nickel foam (Mo-Co(OH) 2 /NF) were developed as a peroxymonosulfate (PMS) activator enabling a pathway transition from radical to non-radical for efficient degradation of organic pollutants. The incorporation of high-valence Mo species promoted the formation of sheet structure and facilitated the Co(II)/Co(III) ratio, while Co served as the primary active site for PMS activation. Consequently, complete removal of 40 mg/L Rhodamine B (RhB) in optimized conditions (catalyst = 1.5 cm 2 , 0.4 g/L PMS dosage, reaction temperature = 25 °C) was achieved within 2 min. In addition, excellent adaptability was exhibited over a wide pH (3.0–9.0) and versatility (99 %, 80.94 % and 91.54 % for MB, LFX, and TC, respectively) in Mo-Co(OH) 2 /NF + PMS system. Impressively, radical scavenging experiments and electron spin resonance (ESR) analyses revealed that the degradation process was mainly dominated by the conversion of O 2 •– to non-radical 1 O 2 . Hence, this work demonstrates the potential of high-valent metal-oxides complexes integrated with Co(OH) 2 as effective PMS activators for non-radical degradation of dye and other refractory antibiotics, significantly broadening their applications in environmental remediation.
研究领域:
环境科学
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材料科学
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化学工程
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DOI
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2022
·
IF 3.322
Tiantian Wang,Ruihe Zheng,Song Sun
Acute lung injury (ALI) is a significant cause of morbidity and mortality worldwide. To search for a new treatment for acute lung injury, we investigated the effect of escitalopram on lipopolysaccharide (LPS)-induced ALI. Our results showed that escitalopram inhibited salt-inducible kinase 2 (SIK2) activity (IC 50 = 6.36 ± 0.93 μM) and triggered histone deacetylase 4 (HDAC4) dephosphorylation . Following its dephosphorylation, HDAC4 translocated into the nucleus, promoted deacetylation and cytoplasmic shuttling of p65, thus inhibited LPS-induced pro-inflammatory cytokine production. Moreover, escitalopram markedly ameliorated the inflammatory responses, reduced neutrophils infiltration and attenuated LPS-induced pulmonary injury in mice. Taken together, we identified a previously unexplored role for escitalopram in SIK2/HDAC4/NF-κB pathway, therefore escitalopram may be considered as a new treatment for ALI.
研究领域:
药理学
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免疫学
·
肺病学
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药物再利用
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Molecular Medicine Reports
·
2023
·Vol. 29
·期 2
·1-11
·
IF 3.4
Xiaoqian Guo,Guangwei Qiao,Jingjiao Wang,Changyi Yang,Min Zhao,Qian Zhang,Yingbiao Wan
Diabetic periodontitis (DP) refers to destruction of periodontal tissue and absorption of bone tissue in diabetic patients. Tumor necrosis factor receptor‑associated factor (TRAF)‑interacting protein with forkhead‑associated domain (TIFA) as a crucial regulator of inflammation activates the NF‑κB signaling pathway to regulate cell biological behavior. However, the function and mechanism of TIFA on DP suffer from a lack of research. In the present study, TIFA was upregulated in the periodontal tissue of a DP mouse model. In addition, the expression of TIFA in RAW264.7 cells was induced by high glucose (HG) culture and increased by lipopolysaccharide (LPS) from Porphyromonas gingivalis treatment in a time‑dependent manner. Knockdown of TIFA significantly reduced the levels of inflammatory cytokines, including TNF‑α, IL‑6, IL‑1β and monocyte chemoattractant protein‑1, in HG and LPS‑induced RAW264.7 cells. The nuclear translocation of NF‑κB p65 was induced by HG and LPS and was clearly suppressed by absence of TIFA. The expression of downstream factors Nod‑like receptor family pyrin domain‑containing 3 and apoptosis‑associated speck‑like protein was inhibited by silencing TIFA. Moreover, TIFA was increased by receptor activator of NF‑κB (RANK) ligand (RANKL) in a concentration dependent manner. The expression of cathepsin K, MMP9 and nuclear factor of activated T cells cytoplasmic 1 was downregulated by depletion of TIFA. RANKL‑induced osteoclast differentiation was inhibited by silencing of TIFA. Meanwhile, the decrease of TIFA blocked activation of the NF‑κB pathway in RANKL‑treated RAW264.7 cells. In conclusion, TIFA as a promoter regulates the inflammation and osteoclast differentiation via activating the NF‑κB signaling pathway.
研究领域:
牙科
·
分子生物学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food & Function
·
2025
·
IF 5.4
Xiaoran Kong,Li Zhao,He Huang,Qiaozhen Kang,Jike Lu,Jia-Qing Zhu
Hyperuricemia is chronic metabolic disease with a high incidence, and it has become the “fourth highest” health risk in modern times. Isorhamnetin is a natural flavonoid found in a variety of plants, especially fruits such as buckthorn. In vivo hyperuricemia ameliorating effect of isorhamnetin and the specific molecular mechanism were profoundly investigated through a hyperuricemia mice model in the present study. The results demonstrated that isorhamnetin showed a significant uric acid-lowering effect in mice. Isorhamnetin was able to reduce uric acid production by inhibiting XOD activity. On the other hand, it reduced the expression of GLUT9 to inhibit uric acid reabsorption and enhanced the expression of ABCG2, OAT1, and OAT3 to promote uric acid excretion. Metabolomics analysis revealed that isorhamnetin gavage restored the purine metabolism and riboflavin metabolism disorders, and thus significantly alleviated the hyperuricemia in mice. Further, the alleviating effect of isorhamnetin on hyperuricemia-induced renal inflammation and its specific mechanism were explored through network pharmacology and molecular validation experiments. Network pharmacology predicted that seven targets were enriched in the PI3K/AKT pathway (CDK6, SYK, KDR, RELA, PIK3CG, IGF1R, MCL1) and four targets were enriched in the NF-κB pathway (SYK, PARP1, PTGS2, RELA). Western blot validated that isorhamnetin inhibited the phosphorylation of PI3K and AKT and down-regulated the expression of NF-κB p65. It indicated that isorhamnetin could inhibit the PI3K/AKT/NF-κB signaling pathway to reduce the levels of renal inflammatory factors (TNF-α, IL-β and IL-6) and ultimately ameliorate the hyperuricemia-induced renal inflammation in mice. This study will provide comprehensive and penetrating theoretical basis for the application of isorhamnetin in the field of functional foods or dietary supplements to improve hyperuricemia.
研究领域:
药理学
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代谢生物学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOLOGICAL & PHARMACEUTICAL BULLETIN
·
2022
·Vol. 45
·期 12
·1733-1742
·
IF 2.264
Yongbin Jing,Mingkun Jia,Jinpeng Zhuang,Dong Han,Changlong Zhou,Jinglong Yan
Osteosarcoma (OS) is the most common primary malignant bone tumor and is mainly diagnosed in children. Toll-like receptor 9 (TLR9) is expressed in various tumor cells and was correlated with cancer progression. However, the underlying mechanism of TLR9 on the OS progression remains unclear. Our previous study demonstrated that the expression of TLR9 was positively correlated with the development stage of OS. Herein, we further evaluated the actual roles and the molecular mechanism of TLR9 on regulating OS cell proliferation and metastasis. Our data showed that TLR9 was upregulated in OS cells compared to normal osteoblastic cells, and knockdown of TLR9 inhibited OS cell proliferation and induced cell cycle arrest by the decreased expression of cyclin D1, CDK2, and p-Rb, while TLR9 overexpression exerted the inverse effects. Furthermore, TLR9 overexpression could enhance the migration and invasion activities of the OS cells by the upregulation of matrix metalloproteinases 2 (MMP2) and MMP9, and the opposite result was observed in TLR9-silenced cells. Moreover, the nuclear factor kappa B (NF-κB) signaling pathway was activated by TLR9, and TLR9-induced malignant phenotype of OS cells was abrogated by the NF-κB antagonist BAY11-7082. Our study indicated that TLR9 might play a critical role in facilitating OS progression by activating the NF-κB signaling pathway, which may provide a valuable therapeutic target for OS.
研究领域:
肿瘤学
·
细胞生物学
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分子生物学
·
癌症研究
✓ 已验证
DOI
PubMed
高影响因子
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