ELECTROCHIMICA ACTA
·
2025
·
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.
✓ 已验证
产品关联
DOI
高影响因子
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Jiao Liu,Danye Niu,Yu Tang,Ruoheng Zheng,Yinyin Qin,Xiuqin Cheng,Shubo Pan,Jinfei Yuan,Xiaohua Shi,Jiao Yang
Background β-Hydroxy β-Methylbutyrate (HMB), derived from leucine, is known for its role in anti-oxidation and anti-inflammation. But, the application of HMB in IBD treatment is not fully understood, highlighting the requirement for further research. Purpose We aimed to examine the effects of HMB treatment on DSS-induced chronic colitis in mice and explore its underlying mechanisms. Methods To simulate colonic inflammation, a murine colitis model was generated by using DSS induction. Critical indicators such as body weight, colon length, disease activity index (DAI), and gross pathology were thoroughly monitored. Immunohistochemistry assay was conducted to assess the expression of Occludin and F4/80. Flow cytometry was employed to evaluate the expression levels of CD80 and CD86. qPCR was performed to measure cytokine expression (IL-6, IL-1β, TNF-α, IL-22, CXCL2, iNOS). RNA sequencing was carried out using bone-marrow derived dendritic macrophage cells (BMDMs). Results Our study indicates that HMB treatment substantially mitigated colonic damage in murine models of DSS-induced colitis, highlighting its anti-inflammatory potential. Notably, HMB significantly enhanced the expression of Occludin in these mice. Furthermore, HMB downregulated proinflammatory markers such as IL-6, IL-1β, and TNF-α as well as CXCL2 in the colon tissue. In vitro experiments also revealed that HMB reduced production of proinflammatory cytokines induced by DSS and suppressed the expression levels of CD80 and CD86 in macrophage cells. On a mechanistic level, we demonstrated the anti-inflammatory effects of HMB by reducing the phosphorylation of p-ERK and p-p65, thereby limiting cytokine production in both in vivo and in vitro settings. Conclusion These findings indicate that HMB possesses anti-inflammation against intestinal inflammation and may hold promise as a potential therapeutic candidate for IBD treatment. There's growing interest in combining traditional anti-inflammatory agents with supplements like HMB to improve outcomes in complex IBD cases. HMB's role in established muscle preservation and reduction of systemic inflammation as described in this study could make it a valuable adjunct in IBD therapy.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF CHEMICAL TECHNOLOGY AND BIOTECHNOLOGY
·
2024
·Vol. 99
·期 12
·2693-2702
·
IF 2.8
Yandong Lu,Jiaxu Ning,Yue Zong,Fu Ding,Gaige Liu,Ruijun Zhang
BACKGROUND Tailored design of high-performance nanofiltration membranes is desirable. The physicochemical properties of the organic phaseare essential for the preparation of nanofiltration membranes. Therefore, byfine-tuning the organic phase, it is possible to achieve nanofiltrationmembranes with enhanced performance. RESULTS In this work, oleic acid, a naturally extracted fatty acid, wasintroduced into three different organic solvents (n-heptane, n-octane andisopar G) to construct special oil phases for interfacial polymerization. Testingresults showed that proper dosage of oleic acid addition can effectivelydecrease the nanofiltration membrane pore size and enhance the salt rejectionregardless of the solvent type. Taking n-octane as example, 5% oleic acidaddition in it can decrease the mean pore size from 0.500 nm to 0.341 nm and improve the MgSO 4 rejection from 52.4% to 95.5%. Further characterizationindicated that the introduction of oleic acid into organic solvent cansignificantly reduce the interfacial tension and promote the diffusion of piperazinefrom aqueous phase to the oil phase. In addition, oleic acid could react with piperazineand produce some white particles that could be embed into the polyamide layer, thus altering the surface morphology. CONCLUSION In this work, a novel modified thin film composite nanofiltration membrane was prepared by a simple and controllable oleic acid assisted interfacial polymerization strategy, which exhibits good water permeability, solute selectivity and antifouling property. Without changing the existing process, our strategy opens up a simple, environmentally friendly and operable route for the synthesis of thin film composite nanofiltration membranes. © 2024 Society of Chemical Industry (SCI).
✓ 已验证
产品关联
DOI
高影响因子
Materials
·
2024
·Vol. 17
·期 10
·2195
·
IF 3.1
Yu Liu,Panpan Li,Zegao Wang,Liangjuan Gao
This study reported a multi–functional Co0.45Fe0.45Ni0.9–MOF/NF catalyst for oxygen evolution reaction (OER), hydrogen evolution reaction (HER), and overall water splitting, which was synthesized via a novel shape–preserving two–step hydrothermal method. The resulting bowknot flake structure on NF enhanced the exposure of active sites, fostering a superior electrocatalytic surface, and the synergistic effect between Co, Fe, and Ni enhanced the catalytic activity of the active site. In an alkaline environment, the catalyst exhibited impressive overpotentials of 244 mV and 287 mV at current densities of 50 mA cm−2and 100 mA cm−2, respectively. Transitioning to a neutral environment, an overpotential of 505 mV at a current density of 10 mA cm−2was achieved with the same catalyst, showing a superior property compared to similar catalysts. Furthermore, it was demonstrated that Co0.45Fe0.45Ni0.9–MOF/NF shows versatility as a bifunctional catalyst, excelling in both OER and HER, as well as overall water splitting. The innovative shape–preserving synthesis method presented in this study offers a facile method to develop an efficient electrocatalyst for OER under both alkaline and neutral conditions, which makes it a promising catalyst for hydrogen production by water splitting.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
International Journal of Electrochemical Science
·
2024
·
IF 1.3
Dandan Liang,Weili Hou,Ying Zhang,Jihua Shang,Haibo Ren,Yufeng Sun
Due to the prevailing energy shortages, the pursuit of new alternative energy sources is becoming increasingly urgent. Hydrogen production through water electrolysis has emerged as a crucial method. However, the sluggish four-electron reaction in the oxygen evolution reaction (OER) remains the primary rate-limiting step. In this study, we synthesized a heterostructure La(OH) 3 @CuO-P material on the nickel foam (NF) substrate. The experimental results demonstrate that after phosphating treatment, the heterostructure La(OH) 3 @CuO-P exhibits exceptional catalytic performance with only 215 mV overpotential, a Tafel slope value of 79.36 mV/dec, and a bilayer capacitance of 39.02 mF/cm 2 at a current density of 10 mA/cm 2 for OER in a 1 M KOH solution. These values are significantly superior compared to those obtained using heterostructure La(OH) 3 @CuO alone which showed an overpotential value of 365 mV at a current density of 10 mA/cm 2 . Moreover, during cyclic voltammetry testing for up to 500 cycles, La(OH) 3 @CuO-P also demonstrates relatively stable performance. Analyses suggest that composite heterostructure effectively addresses issues such as insufficient conductivity of La(OH) 3 and monomer aggregation tendency for CuO while maintaining excellent properties for each component. By incorporating P atoms as dopants, the interaction between La, Cu, and P atoms not only facilitates fine-tuning of the electronic structure and optimization of the adsorption free energy (-OH), but also promotes an increase in catalytic active sites through sample size reduction, thereby further augmenting the performance of the OER.
✓ 已验证
产品关联
DOI
高影响因子
Hepatology International
·
2025
·
IF 6.1
Yang Yanfang,Wang Tao,Fu Yuyin,Li Xukui,Yu Fuxun
Background Hepatitis B virus (HBV) is a pathogen that poses a serious threat to human health. The interaction between HBV and host has made great progress in recent years. SUMOylation is involved in virus-related cancer progression, but there are fewer studies on the mechanism of SUMOylation on HBV replication and antiviral defense. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a critical adaptor of the NF-κB pathways. Here, we focus on the roles of TRIM28 in regulating TRAF6 SUMOylation in HBV-replicating cells. Methods The SUMO1-modified TRAF6 proteins were enriched from total cellular proteins by immunoprecipitation with anti-SUMO1 antibody, then the SUMOylated TRAF6 was detected by western blot using an anti-TRAF6 antibody. The interaction between TRAF6 and TRIM28 was identified by immunoprecipitation and LC–MS/MS. The modification sites of TRAF6 SUMOylation were identified by amino acid site mutation. Expression and localization of TRAF6 and TRIM28 were assessed by immunohistochemistry and immunofluorescence. The hydrodynamic injection HBV mouse model was used to determine the function of TRIM28-mediated TRAF6 SUMOylation in vivo. Results The results show that the levels of SUMO1-modified TRAF6 are elevated in HBV-replicating cells. Lys453 is a major SUMO1 modification site of TRAF6. There is an antagonistic interaction between SUMOylation and ubiquitination of TRAF6 protein. The SUMO ligase TRIM28 is responsible for catalyzing TRAF6 SUMOylation. Compared to the wild-type TRAF6, its SUMO site mutant TRAF6 K453R promotes NF-κB activation. Moreover, TRIM28 overexpression attenuates TRAF6-mediated NF-κB activation, thereby inhibiting HBV replication in vivo. Conclusions Our findings demonstrate that SUMO ligase TRIM28 affects the ability of TRAF6 on NF-κB activation, nucleocytoplasmic shuttling and HBV replication-related indicators. Our data reveal that TRIM28-mediated SUMOylation of TRAF6 is a novel mechanism to regulate the inflammatory response, which may pave the way for new strategies to control anti-HBV.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）