INFLAMMATION
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2026
·Vol. 49
·期 1
·41
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IF 5
Zheng-qing Hu,Ruijie Ma,Hang Zhang,Jiahao Miao,Jia-qing Sun,Jinlong Yuan,Jiaqiang Liu,Zihuan Zhang,Dayong Xia
This study aims to elucidate the mechanism by which Heat Shock Protein 60 (HSP60) mediates microglial pyroptosis in the context of early brain injury (EBI) following subarachnoid hemorrhage (SAH), and to investigate the effects of HSP60 inhibition on EBI after SAH. A mouse subarachnoid hemorrhage (SAH) model was established using prechiasmatic cistern blood injection. In vitro, microglia were stimulated with 25 µmol/L oxyhemoglobin (OxyHB) to simulate the SAH pathological environment. In vivo, mice received 100 mg/kg Mizoribine, while in vitro, 80 µmol/L Mizoribine was used to suppress SAH-induced HSP60 upregulation. Techniques including Western blotting, immunofluorescence, immunohistochemistry, transmission electron microscopy, ELISA, modified Garcia neurological scoring, beam walking, brain water content measurement, Morris water maze, TUNEL staining, and Nissl staining were employed to systematically investigate the role of HSP60 inhibition in neuroinflammation and microglial pyroptosis after SAH. Compared to the sham group, both in vivo and in vitro studies with blinded, random sampling of six groups demonstrated a significant increase in HSP60 expression post-SAH. In vivo, 100 mg/kg Mizoribine alleviated blood-brain barrier disruption, cerebral edema, neuronal apoptosis/necrosis, and improved neurological deficits and cognitive impairment. In vitro, 80 µmol/L Mizoribine markedly attenuated microglial activation and pyroptosis, downregulated pro-inflammatory cytokines, and mitigated neuroinflammation. The upregulation of HSP60 after SAH promotes NLRP3 inflammasome assembly by activating the TLR4/MyD88/NF-κB signaling pathway, thereby inducing microglial pyroptosis and exacerbating the progression of early brain injury. Inhibition of HSP60 represents a potential therapeutic strategy for ameliorating EBI after SAH.
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
·
IF 5.4
Aoyu Zhang,Shuying Li,Jie Qiao,Chuanqi Zhong,Zhiwen Zhang,Xiguang Ye,Jun Jin,Shiyan Shang,Song Wu,Qing Zhang,Gongxu Yang
Ethnopharmacological relevance The therapeutic effect of Psoralea corylifolia L. on knee joint pain was recorded as early as the Ming Dynasty in the Compendium of Materia Medica, which notes its actions of tonifying the kidney, strengthening tendons, and bones. Isopsoralen (ISO), derived from the Psoralea corylifolia L., has shown efficacy in improving osteoarthritis (OA) in both traditional use and our previous screening, demonstrating effects in alleviating joint inflammation and protecting cartilage. Aim of the study OA is a common disabling disease. Its progression connects local joint pathology to systemic metabolic and inflammatory states, extending to gut microbiota and metabolites. This study examines the therapeutic mechanism of isopsoralen against OA using a DMM-induced model. Materials and methods ISO's targets were predicted by network pharmacology approaches. Therapeutic effects were evaluated through behavioral tests, micro-CT, histology, Western blot, and PCR, while safety was assessed via liver/kidney staining. 16S rDNA sequencing and targeted metabolomics were employed to analyze gut microbiota structure and short-chain fatty acids (SCFAs). Pseudo germ-free mice and fecal microbiota transplantation (FMT) were used to validate the role of gut microbiota. Results Network pharmacology indicated ISO's multi-target action against OA. ISO downregulated the MAPK/NF-κB pathway, attenuated subchondral bone abnormalities, and alleviated joint degeneration in DMM mice. It also modulated gut microbiota composition and SCFA levels. FMT confirmed the essential role of gut microbiota in ISO's efficacy. Furthermore, no hepatorenal toxicity was observed. Conclusion ISO alleviates OA by modulating gut microbiota/SCFAs and inhibiting the MAPK/NF-κB pathway, thereby reducing inflammation and improving bone abnormalities, without hepatorenal toxicity.
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Frontiers in Molecular Biosciences
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2026
·
IF 4
Xingwei Yu,Hongao Tan,Yunqiu Gao,Dandan Qiu,Yan Zhu,Haixin Qi
Background: Given the lack of effective treatment for chronic nonbacterial prostatitis (CNP) and the anti-inflammatory property of natural bioactive compound forsythiaside A (FTA), the therapeutic potential of FTA on CNP is worthy of investigation.Methods: CNP rat models were established using complete Freundʼs adjuvant, followed by a 4-week administration of FTA at different concentrations (40 and 80 mg/kg/d). The body and prostate of rats were weighed to calculate the prostatic index. Prostate damage and inflammatory infiltration were assessed using histological analysis and immunohistochemistry staining. Levels of inflammation-related cytokines, autophagic markers as well as the protein kinase C alpha (PKCα)/NF-κB pathway in prostate tissues were detected using enzyme-linked immunosorbent assay and western blot.Results: No significant change was observed in the body weight of CNP rat models administered with or without FTA. FTA treatment reduced the prostatic index and mitigated prostate damage and inflammatory infiltration of CNP rat models. FTA treatment decreased the number of CD3-positive cells and CD45-positive cells, while downregulating interleukin 1 beta (IL-1β), IL-2, IL-6, IL-17A, monocyte chemoattractant protein-1, and tumor necrosis factor alpha in prostate tissues of CNP rat models. FTA treatment promoted Beclin-1 and LC3B II/LC3B I expressions, and inhibited PKCα and p-p65/p65 expressions in prostate tissues of CNP rat models.Conclusion: FTA alleviates inflammation and facilitates autophagy in CNP rat models by blocking the PKCα/NF-κB pathway.
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JOURNAL OF ALLOYS AND COMPOUNDS
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2026
·
IF 6.3
Yi Zheng,Yibai Sun,Qi Wang,Ronghui Xu,Yingping Zheng,Jinxi Chen,Yongbing Lou
The design of an efficient oxygen evolution reaction (OER) catalyst is significant for water splitting. Telluride-based materials exhibit exceptional electrical conductivity and mass transfer properties, yet their application in electrocatalysis remains constrained by limited active site exposure. Conversely, layered double hydroxides possess unique granular/lamellar morphologies that offer significant potential for active site amplification through strategic morphology regulation. In response to the demand for highly efficient and stable OER electrocatalysts, this study presented a rationally designed heterostructure. NiTe nanorods were first grown on nickel foam (NF), followed by intimate coupling with granular nickel-copper layered double hydroxide (NiCu-LDH). Ultimately, a well-defined core-shell structure of NiCu-LDH/NiTe@NF was successfully constructed. Unlike conventional 2D nanosheets, the NiCu-LDH exhibited unique low-crystallinity characteristics, resulting in a crystalline-amorphous heterostructure that provided abundant unsaturated coordination sites, thereby effectively facilitating the adsorption and conversion of reaction intermediates. Benefiting from the optimized interfacial electronic structure and rapid charge transfer capability, the composite catalyst exhibited an overpotential of only 315 mV at a current density of 100 mA cm −2 and maintained stable operation for over 160 h at 50 mA cm −2 with negligible performance degradation. Mechanistic studies revealed that the formation of NiOOH acts as the true active species, significantly enhancing OER performance. This work not only offered a high-performance OER electrocatalyst, but also provided new insights into the rational design of crystalline-amorphous composite materials.
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POULTRY SCIENCE
·
2026
·
IF 4.5
Jie Qi,Haotian Yang,Yang Yang,Xinyi Dou,Xin Chen,Qiuyue An,Tingyang Wu,Xiuzhi Liu,Yu Boyuan,Hao Wang,Siqi Wang,Yinkang Song,Chenjia Shi,Chao Ma,Jia Chen,Yuan Zhao,Honggang Fan
This study evaluated the effects of esculetin on heat stress-induced splenic immunosuppression in broilers. Esculetin significantly reduced rectal temperature and respiratory rate in heat-stressed broilers ( P < 0.05), improved growth performance, serum biochemical parameters, and the spleen index, and attenuated heat stress-induced splenic histopathological damage and HSP70 expression. Concurrently, esculetin elevated serum levels of immunoglobulins (IgA, IgM, and IgG) and upregulated the gene expression of anti-inflammatory cytokines, while downregulating pro-inflammatory cytokine genes (IL-1β, IL-6, and TNF-α). Network pharmacology analysis, molecular docking, and in vivo validation demonstrated that the immunomodulatory effects of esculetin were primarily mediated through targeting NF-κB, TNF-α, and IL-6, thereby modulating the NF-κB/MAPK signaling pathway. These findings provide a scientific basis for the application of esculetin as a functional feed additive to alleviate heat stress-induced immune dysfunction in poultry.
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POULTRY SCIENCE
·
2026
·Vol. 105
·期 12
·107847
·
IF 4.5
Shunxing Liu,Yanling Xiong,Zhentao Cheng,Anchun Cheng,Rutao Lin,Hui Li,Yao Huang,Binlan Zhou,Ting Yang,Chunlan Shan
Mycoplasma gallisepticum ( MG ), a significant pathogen, causes chronic respiratory disease (CRD) in poultry, characterized by coughing, wheezing, and dyspnea. This widespread disease severely impedes the healthy development of the poultry industry. Hydroxytyrosol (HT), a plant-derived monomeric compound, possesses diverse bioactivities, including antibacterial, antioxidant, and cardiovascular protective properties. This study aimed to investigate HT's protective effect against MG -induced inflammatory damage in HD11 cells. The findings revealed that MG infection activated the TLR4/NF-κB signaling pathway and the NLRP3 inflammasome, resulting in macrophage accumulation and inflammatory damage in the lung tissue of chicks. HT mitigated MG -induced inflammatory damage in HD11 cells, inhibited the M1 phenotype shift, and reduced the secretion of pro-inflammatory factors. Molecular docking and molecular dynamics simulations demonstrated HT's stable, spontaneous binding to NLRP3. Further investigations showed that HT alleviates oxidative stress-induced cellular damage, diminishes pathological apoptosis and pore formation, and concurrently reduces NLRP3 activation by regulating the TLR4/NF-κB pathway, thereby downregulating the expression of key pyroptosis factors. In summary, HT reduces NLRP3 inflammasome activation by specifically inhibiting the TLR4/NF-κB signaling axis, consequently alleviating inflammation-induced damage, oxidative stress, and pyroptosis in HD11 cells caused by MG infection.
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Catalysts
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2026
·Vol. 16
·期 5
·428
·
IF 4.5
Jianlong Wen,Yuan Yu,Dongfeng Sun,Yanning Qu,Xiaoya Yuan,Congcong Lin,Jia Liu,Yiyan Jiang,Yunkun Yang,Bingshe Xu
A layered bimetallic CoMo-LDH precursor was prepared on nickel foam via a hydrothermal method, and a 3D hierarchical flower-like nanosheet CoMoP/NF electrocatalyst with a crystalline–amorphous heterostructure was constructed in situ through low-temperature phosphidation. The water electrolysis performance was optimized by adjusting the Co/Mo molar ratio. The 3D hierarchical porous structure provides a large specific surface area and abundant active sites, and Mo doping effectively modulates the electronic structure. The catalyst exhibits superior HER performance with overpotentials of only 37 mV and 65 mV at 10 mA·cm−2in acidic and alkaline media and shows a lower HER overpotential than commercial Pt/C at current densities above 426 mA·cm−2in acidic conditions. Meanwhile, this catalyst delivers an OER overpotential of 729 mV at 500 mA·cm−2in alkaline media and can operate stably for 50 h. The assembled two-electrode overall water splitting cell only requires 1.42 V at 10 mA·cm−2, outperforming Pt/CǁRuO2(1.52 V). This work offers a promising strategy for designing low-cost and high-efficiency overall water splitting electrocatalysts for high-current-density applications.
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Food & Function
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2026
·
IF 6.3
Ziyuan Zhou,Xiaxia Pan,Jiali Ni,Zhuoqi Lou,Yangfan Shen,Shiman Jiang,Xiangmin Dong,Fengjiao Wang,Yanfei Chen,Lanjuan Li
Existing evidence indicates that pre-existing metabolic dysfunction-associated steatotic liver disease (MASLD) confers susceptibility to acute liver injury (ALI). Nevertheless, the underlying mechanism prompting ALI risk in such condition is not fully uncovered yet. Gut dysbiosis has been well-documented in MASLD patients which prompts us to hypothesize that gut dysbiosis may serve as a contributing factor and regulating target to ALI susceptibility. A case-control study was performed and verified the increased risk of ALI in MASLD patients. Mice pretreated with MASLD mice/patients-derived fecal microbiota transplantation (FMT), demonstrated worsened ALI after D-GalN/LPS injection. We identified significant gut dysbiosis with decreased microbial α-diversity, beneficial genus lactobacillus, increased potential harmful bacteria Campylobacter and helicobacter. Probiotic Akkermansia muciniphila (A. muciniphila) was reported to improve gut dysbiosis. Thus, we tested the effect of A. muciniphila on ALI mice pretreated with MASLD mice-derived FMT. A. muciniphila significantly ameliorated the worsened ALI and improved gut dysbiosis. Transcriptomic analysis reveled that A. muciniphila restored the impaired liver PPAR-α signaling, alleviating the aggravated NF-κB signaling and downstream inflammation response in liver. Specifically, A. muciniphila restored the decreased abundance of PPAR-α agonist daidzein in colon, thereby restoring PPAR-α activation and inhibiting NF-κB signaling in liver. Daidzein is also capable to ameliorate ALI aggravated by MASLD-associated dysbiosis, accompanied by PPAR-α activation and NF-κB inhibition. Our findings revealed that gut dysbiosis in MASLD increased the risk of ALI. A. muciniphila exhibited preventive potential for MASLD patients to reduce ALI risk. Daidzein/PPAR-α/NF-κB signaling is important to maintain host resistance to hepatoxic challenge.
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Toxicology Research
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2026
·Vol. 15
·期 1
·
IF 2.9
Yang Haoming,Yin Yuan,Wang Pengkai,Li Jiakai,Yuan Fang,Xiang Debiao,Deng Yang,Li Xin
Polymyxin B remains a first-line therapeutic option against Gram-negative bacterial infections; however, its clinical utility is substantially limited by dose-limiting toxicity, the mechanisms of which remain incompletely elucidated. Within a network toxicology framework, this study systematically investigated the potential toxic characteristics and underlying molecular mechanisms of Polymyxin B, with a specific focus on three key adverse effects: acute kidney injury, neurotoxicity, and skin pigmentation. Potential targets associated with Polymyxin B exposure and these toxicities were initially identified through integrated data mining of the SuperPred, SEA, GeneCards, and OMIM databases. A protein–protein interaction (PPI) network was subsequently constructed and analyzed using the STRING database and Cytoscape software. Functional enrichment analyses, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses, were performed using Metascape. Furthermore, a compound–target–pathway network and Sankey diagram were generated to identify major active components, followed by molecular docking between these components and proteins encoded by the key targets. Molecular docking and molecular dynamics simulations confirmed strong binding affinities between Polymyxin B and core target proteins, namely STAT3, NF-κB, PRKACA, and HIF1A. Notably, both PMB1 and PMB2 exhibited high binding affinity for NF-κB. Consistent with these findings, in vivo studies in mice demonstrated that Polymyxin B treatment significantly enhanced the activation of the NF-κB pathway in renal tissues. Conversely, co-administration of the NF-κB pathway inhibitors PDTC and JSH-23 markedly attenuated Polymyxin B-induced nephrotoxicity. In conclusion, these experimental results indicate that hyperactivation of NF-κB is a critical mechanism underlying Polymyxin B-induced renal toxicity.
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Journal of Materials Chemistry A
·
2026
·
IF 9.2
Qingyuan Song,Jinshou Yao,Liujun Jin,Peiyang Gu,Ye Wang,Ping Liu,Congping Chen,Guohong Dai
Dibutyl phthalate (DBP), a ubiquitous plasticizer pollutant, poses severe risks to environmental and human health, yet its high chemical stability makes valorization highly challenging. Herein, we report a one-pot, mild, and green strategy that directly upcycles DBP as an organic ligand to construct a ferroferric oxide functional Ni-based MOF framework nanocomposite (Fe3O4-Ni-MOF(DBP)) on nickel foam (NF), enabling the simultaneous detoxification of DBP and fabrication of a high-performance electrocatalyst. The in-situ integration of Fe3O4 nanoparticles with the Ni-MOF(DBP) endows the hybrid catalyst with accelerated charge-transfer kinetics, enhanced electrical conductivity, and abundant accessible active sites, leading to remarkable bifunctional activity for overall water splitting. In an alkaline electrolyte, Fe3O4-Ni-MOF(DBP)/NF exhibits outstanding bifunctional electrocatalytic performance, delivering low overpotentials of 233 mV for the OER and 42 mV for the HER at 10 mA cm -2 , along with excellent durability over continuous operation exceeding 40 h. In-situ Raman analysis reveals that the superior catalytic performance of Fe3O4-Ni-MOF(DBP)/NF is attributed to the dynamic reconstruction of surface metal sites into active (oxy)hydroxide intermediates. This work presents an innovative strategy for the valorization of toxic plastic pollutants, thus advancing the cross integration of environmental remediation and clean energy technologies.
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JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2026
·Vol. 40
·期 8
·e71058
·
IF 3.6
Yongmei Li,Yuexin Xu,Wenjie Ye,Zeqi Yu,Zhenkun Wu,Xinyi Liu,Xuhong Huang,Jianxin Pang,Zean Zhao,Ting Wu
Hyperuricaemia (HUA) is a recognized risk factor for cardiovascular and renal diseases. Isobavachin, a dihydroflavone derivative, demonstrates significant efficacy in reducing uric acid levels. This study investigated the nephroprotective and cardioprotective effects and molecular mechanisms of isobavachin. Through integrative network pharmacology, pathway enrichment analysis, and molecular docking, NF‐κB was identified as a potential target of isobavachin in the context of hyperuricemia‐related cardiac and renal injury. Isobavachin treatment inhibited the activation of the NF‐κB pathway, leading to cytoprotection in uric acid (UA)‐stimulated mRTEC and H9C2 cells. In chronic HUA mice, isobavachin treatment significantly improved renal pathology and reduced renal collagen deposition by inhibiting epithelial‐to‐mesenchymal transition. Isobavachin administration demonstrated therapeutic efficacy in attenuating myocardial injury, hypertrophy, and fibrotic remodeling. Notably, the anti‐inflammatory effects of isobavachin were particularly evident in both renal and cardiac tissues, primarily mediated through its dual regulatory capacity in suppressing NF‐κB pathway activation and NLRP3 inflammasome formation. In conclusion, isobavachin ameliorated cardiac and renal damage caused by chronic HUA, suggesting a new strategy to prevent HUA. Isobavachin alleviates HUA‐induced oxidative stress, inflammation, and fibrosis in the kidney and heart, potentially through its dual role in promoting UA excretion and inhibiting NF‐κB signaling and NLRP3 inflammasome activation.
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JOURNAL OF PHYSICS AND CHEMISTRY OF SOLIDS
·
2026
·
IF 5.9
Yadong He,Changsheng Tang,Zhangyong Li,Shu Zhao,Yixin Kang,Yangxin Zhang,Xinzhan Wang,Ling Li
A hierarchical CCO@ZWO core-shell architecture was fabricated on nickel foam. • Binder-free CCO@ZWO/NF electrode delivers 3670 mF cm −2 at 1 mA cm −2 . • The CCO@ZWO/NF//AC/NF ASC retains 87.75% capacitance after 7800 cycles. • The ASC device achieves 0.198 mWh cm −2 at 0.75 mW cm −2 . One heavily relied-upon strategy for achieving advanced electrode materials with superior properties for asymmetric supercapacitors (ASCs) is the rational design of hierarchical core-shell heterostructures on conductive substrates. In this work, a well-defined urchin-like CuCo 2 O 4 @ZnWO 4 (CCO@ZWO) core-shell heterostructure was successfully fabricated on porous nickel foam (NF) via a simple two-step solvothermal process, followed by thermal annealing. The hierarchical structure is composed of CuCo 2 O 4 nanoneedles serving as the conductive core, with ZnWO 4 nanosheets uniformly anchored as the shell layer, which collectively provides an extensive specific surface area with a high density of electroactive centers and favorable ion/electron transport kinetics. With a binder-free architecture, the CCO@ZWO/NF composite delivers a high areal capacitance of 3670 mF cm −2 at a current density of 1 mA cm −2 , enabling the assembly of an asymmetric supercapacitor with CCO@ZWO/NF as the positive electrode and NF-supported activated carbon as the negative electrode. The device exhibited a cycling stability that was evaluated over 7800 cycles at 4 mA cm −2 , showing a capacitance preservation of 87.75%, while a capacitance per unit area of 633.7 mF cm −2 was obtained at 1 mA cm −2 . The remarkably improved electrochemical performance stems from the cooperation between the two components and the robust core-shell architecture, which effectively mitigates volume expansion and structural collapse during repeated cycling. These findings underscore the considerable promise of the designed CCO@ZWO core-shell heterostructure in serving as an advanced electrode material, offering a viable pathway for exceptional energy storage applications. A biomimetic urchin-like CuCo 2 O 4 @ZnWO 4 core-shell heterostructure was grown on nickel foam via a two-step solvothermal method with subsequent annealing. The hierarchical architecture provides a large specific surface area, abundant active sites, and fast ion/electron transport. The CCO@ZWO/NF electrode delivers a high areal capacity of 3670 mF cm −2 at 1 mA cm −2 , and the ASC device achieves an energy density of 0.198 mWh cm −2 with 87.75% retention after 7800 cycles. This superior performance stems from the synergistic interplay between the core-shell morphology and the multi-metal oxide composition. Download: Download high-res image (352KB) Download: Download full-size image
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