NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
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2026
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IF 4
Chen Haiyang,Zhang Lijun,Liu Meiyan,Li Yanwei,Wei Dajian,Wei Jingjing,Li Xiaofeng,He Dongfang,Chi Yunpeng
Acute myocardial infarction (AMI) and insomnia are mutually causal. However, therapeutic strategies for AMI combined with insomnia remain limited. Mechanistically, parachlorophenylalanine (PCPA)-induced sleep deprivation (SD) exacerbates AMI by activating the sympathetic nervous system and triggering systemic inflammatory responses. However, the specific cascade through which PCPA-induced SD-mediated systemic inflammation aggravates myocardial injury remains unclear. Bisoprolol amlodipine tablet (BAT), containing bisoprolol and amlodipine, exerts cardiovascular protective effects, in which bisoprolol mitigates sympathetic overactivation, while amlodipine alleviates AMI-related inflammatory responses. Shumian capsule (SMC) improves sleep quality with potential anti-inflammatory and neuroprotective properties. Given the complementary mechanisms of BAT and SMC, and the unmet clinical need for safe, effective therapies targeting AMI-insomnia comorbidity, this study aims to explore the therapeutic mechanisms of BAT combined with SMC on myocardial injury induced by AMI and PCPA-induced SD, providing novel insights for clinical practice. Male Sprague Dawley rats were randomly divided into five groups: sham, MI, MI + SD, BAT, and BAT + SMC. The MI model was established by ligating the left anterior descending coronary artery, and the SD model was induced by intraperitoneal injection of parachlorophenylalanine. After model establishment, rats in the BAT group received BAT (1.05 mg/kg, i.g.), and those in the BAT + SMC group received BAT combined with SMC (252 mg/kg, i.g.) for one week. Behavioral tests, echocardiography, heart rate, heart weight (HW)/body weight (BW), HW/tibia length (TL), histopathological staining, immunofluorescence co-localization, ELISA, qRT-PCR, and Western blot were used to evaluate anxiety- and depression-like behaviors, cardiac function, tissue injuries, inflammatory responses, and related gene and protein expression. PCPA-induced SD mediated the aggravation of MI-induced anxiety and depression-like behaviors, hippocampal and myocardial pathological injuries, myocardial fibrosis, apoptosis, and cardiac dysfunction in rats. It also increased the levels of myocardial injury biomarkers and inflammatory cytokines, and was accompanied by elevated activation status of the Panx1/P2X7 pathway, which may correlate with promoted neutrophil recruitment and changes in NETosis-related markers. Compared with monotherapy with BAT, the BAT combined with the SMC group showed more favorable alterations across all measured parameters. Compared with monotherapy with BAT, the combination of BAT and SMC showed more favorable alterations in all measured parameters. BAT combined with SMC improved the sucrose preference index and locomotor activity, ameliorated neuronal and dendritic injuries in the hippocampus, increased left ventricular ejection fraction and shortening fraction, reduced left ventricular end-diastolic and end-systolic diameters, HR, HW/BW, and HW/TL, alleviated myocardial fibrosis and apoptosis, decreased the levels of CK-MB, cTnI, TNF-α, and IL-1β, was correlated with suppressed expression of Panx1 and P2X7, and presented lower levels of NETosis-related markers (MPO, NE, and Cit-H3). BAT combined with SMC may alleviate myocardial injuries in rats with AMI and PCPA-induced SD via alterations to the Panx1/P2X7 pathway-associated changes in NETosis-related markers. This combined intervention integrates the cardiovascular-protective actions of BAT with the sleep-improving and neuroprotective properties of SMC, which may help relieve the vicious cycle of PCPA-induced SD-triggered inflammation and myocardial damage. Our findings reveal a molecular link between the Panx1/P2X7-associated changes in NETosis-related markers and the therapeutic benefits of BAT and SMC combination therapy, and provide preclinical evidence for its potential translation into clinical practice. This innovative treatment strategy offers a safe and effective alternative for managing AMI patients with concurrent insomnia, addressing a critical unmet medical need.
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高影响因子
Nature Communications
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2026
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IF 18.1
Jun Pang,Xinyu Bai,Junjie Dai,Sijie Liu,Shuangfeng Yin,Yong Pei,Rong Tan
Artificial photosynthesis of acetaldehyde from atmospheric CO 2 is highly promising, yet remains severely limited by low CO 2 concentration in air and sluggish proton transfer kinetics. Herein, we report metallo hydrogen-bonded organic frameworks (MHOFs) of HNNU-X (X = O, S, Se) which enable acetaldehyde synthesis directly from air, water, and natural sunlight. Among them, HNNU-Se exhibits a competitive acetaldehyde production rate of 557.1 μmol g⁻¹ h⁻¹ with high electron-based selectivity of 95% under outdoor conditions, without need of sacrificial agents. Mechanistic studies reveal that HNNU-X creates a proton-rich microenvironment in which [Zn(tpy)] 2+ cations function as CO 2 capture and activation sites for direct air capture, while [XCN] – anions serve as proton shuttles, facilitating rapid transfer of in-situ generated H⁺ from solar-driven water oxidation to adsorbed CO 2 . This work enables the synergistic coupling of CO 2 reduction and H 2 O oxidation, thereby achieving efficient artificial photosynthesis of acetaldehyde. This study develops metallo hydrogen-bonded organic frameworks (HNNU-X), which overcome the low CO 2 concentration in air and sluggish proton transfer kinetics, achieving artificial photosynthesis of acetaldehyde from air, water and natural sunlight.
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PubMed
高影响因子
npj Science of Food
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2026
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IF 9.7
Xie Shufu,McClements David Julian,Hong Qing,Liu Zhenmin,Zhang Zipei,Qiu Chao,Zhao Jianwei,Jin Zhengyu,Chen Long
With global aging, intestinal homeostasis disruption contributes to inflammation, oxidative stress, and metabolic disorders. This study assessed fucoidan at doses of 100, 250 and 500 mg/kg in aged mice. The high dose (500 mg/kg) improved food intake, body weight and intestinal transit, and elevated α-amylase activity. It also relieved oxidative stress, strengthened intestinal tight junctions and restored mucosal morphology. Multi-omics analyses revealed that fucoidan reshaped the gut microbiome—enriching beneficial taxa (e.g., Akkermansia ) while suppressing opportunistic pathogens—and increased short-chain fatty acid production. Untargeted metabolomics indicated enrichment of antioxidant and barrier-protective metabolites and clearance of cytotoxic compounds, with key impacts on amino acid, lipid, and energy metabolism. Overall, fucoidan systematically restores aging intestinal homeostasis via a “microbiota–metabolite–host” axis, supporting its potential as an anti-aging functional food.
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CELL DEATH AND DIFFERENTIATION
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2026
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IF 13.6
Tang Tianyu,Yang Wuping,Lu Minghao,Peng Ding,Li Shiqi,Cui Sijia,Ye Sunyi,Liu Jiandong,Wang Yifan,Wu Cunjin,Teng Haoyang,Huang Haojie,Xu Xin,Xia Dan,Zhu Yi
Aberrant tumor metabolism plays a crucial role in establishing and sustaining an immunosuppressive microenvironment. CD73, a key enzyme in the purine metabolism pathway, is frequently overexpressed in tumors, leading to elevated extracellular adenosine (ADO) levels. This accumulation suppresses antitumor immune responses by promoting immune cell exhaustion, ultimately contributing to immunotherapy resistance. However, the mechanisms underlying CD73 upregulation in tumors remain poorly defined. Here, we identify aurora kinase B (AURKB) as a critical regulator of CD73 overexpression in renal cell carcinoma (RCC), orchestrating immune evasion and resistance to immune checkpoint therapy. AURKB is highly expressed in RCC, with its prognostic significance being especially evident in tumors with strong immunogenicity. Mechanistically, AURKB enhances CD73 expression, thereby promoting T cell dysfunction and immune suppression. Mass cytometry (CyTOF) analysis revealed that AURKB inhibition facilitates immune infiltration and alleviates immune exhaustion. We further demonstrate that AURKB directly interacts with CD73 and phosphorylates it at serine 429, which inhibits STUB1-mediated ubiquitination and proteasomal degradation of CD73. Targeting AURKB to modulate the post-translational stability of CD73 restores antitumor immunity and synergizes with immune checkpoint blockade in vivo. Collectively, this study uncovers a previously unrecognized AURKB–CD73 axis and provides a mechanistically informed strategy to enhance immunotherapy efficacy in RCC.
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Microbiome
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2026
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IF 14.9
Fu Yang,Yin Nuoming,Huang Zehua,Qin Wenfei,Xu Binqiang,Huang Huizhen,Hu Jia,Cui Mengyan,Mei Qixiang,Fan Junjie,Lu Yingying,Jiang Qiaoli,Hu Junjie,Huang Chunlan,Zeng Yue
Background Gut barrier dysfunction is critical in the pathogenesis of acute pancreatitis (AP), yet the underlying mechanisms remain unclear. Mucin 2 (MUC2), the primary component of the intestinal mucus layer, is essential for gut homeostasis and microbial eubiosis. This study aimed to elucidate the protective mechanism of intestinal MUC2 in AP. Results We reported that intestinal MUC2 expression was decreased in AP patients and correlated with disease severity. Intestinal epithelial-specific Muc2 knockout ( Muc2 ΔIEC ) mice demonstrated exacerbated AP in a gut microbiota-dependent manner. Decreased abundance of Lactobacillus and correlated reduced levels of riboflavin were found in Muc2 ΔIEC mice after AP induction. Supplementation with riboflavin effectively ameliorated AP in Muc2 ΔIEC mice, whereas administration of an engineered strain deficient in riboflavin synthesis failed to provide a protective effect. MUC2 deficiency aggravated a macrophage-dominant immune imbalance in the pancreas, which was reversed by riboflavin. In vitro experiments revealed that riboflavin suppresses pro-inflammatory macrophage activation by inhibiting the CD40 signaling pathway. This inhibition preserved mitochondrial function and reversed the histone H3 acetylation at pro-inflammatory gene promoters. Conclusion Our study demonstrates that intestinal MUC2 deficiency is associated with reduced levels of microbiota-derived riboflavin, which could partially suppress pro-inflammatory macrophage activation via the CD40 pathway. Targeting the microbiota-derived riboflavin in AP may help to ameliorate the disease course.
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高影响因子
CATALYSIS LETTERS
·
2026
·Vol. 156
·期 9
·248
·
IF 2.5
He Jiayao,Liu Shuxin,Tian Xiaoxia,Zhao Jiuzhou,Xian Liang
In this study, a porous carbon support (CuCN) with a high specific surface area and an N-doped Cu-N-C network was synthesized by pyrolyzing copper acetylacetonate on a metal-organic framework (ZIF-8) at 900 °C. To investigate the relationship between the preparation process and performance of CuCN-supported palladium nanoparticles, a light-induced synthesis method was employed to replace the traditional high-temperature thermal reduction process, enabling the controlled loading of palladium nanoparticles onto CuCN. A Cu- and N-co-doped carbon-supported palladium nanocatalyst (Pd/CuCN-M) was prepared, and the effects of optimal illumination conditions and reducer types on the catalyst were explored. The results show that the Cu- and N-co-doped carbon-supported palladium nanocatalyst, designated Pd/CuCN-M1, prepared using methanol as the reducing agent and irradiated with near-ultraviolet light at 395 nm, exhibits high catalytic activity and stability. The rate constant for the reduction of p-nitrophenol (4-NP) reached 2.1 min⁻¹, and the conversion rate remained at 90.2% after five cycles of stability testing. This study presents a green, convenient, and highly efficient method for synthesizing Pd nanocatalysts, offering a new approach to reducing the use of precious metals and treating p-nitrophenol-based pollutants generated in industrial production. Graphical
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MICROCHIMICA ACTA
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2026
·Vol. 193
·期 8
·559
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IF 5.4
Wu Minjin,Yu Wenzhan,Xu Yue,Zou Guangrui,Huang Zihao,Li Ling,Li Jianping
A self-enhancing Cu-TBAPy MOF was synthesized, which serves as both an electrochemiluminescence (ECL) emitter and a dual coreactant accelerator. It was then employed as an ECL probe to construct a highly sensitive ECL immunosensor for the sensitive determination of the lung cancer marker Cyfra 21 − 1. Benefiting from its rigid framework structure and the spatial confinement of the TBAPy ligand imposed by Cu 2+ coordination, thermal dissipation of the excited-state energy from the ligand is effectively suppressed, resulting in a strong ECL signal that renders this material suitable as a probe for ECL immunosensors. Moreover, the Cu 2+ sites within the MOF catalyze the reduction of K 2 S 2 O 8 at the electrode to produce the coreactant SO 4 •‒ . Meanwhile, the MOF exhibits peroxidase-like activity, catalyzing the reduction of H 2 O 2 to generate hydroxyl radicals (OH • ), which further react with K 2 S 2 O 8 to yield additional SO 4 •‒ . Through the dual promotion mechanism, the ECL signal of the MOF is substantially enhanced. The Cu-TBAPy MOF was employed as a probe, and secondary antibody‑labeled polydopamine nanospheres (PDA NPs) were introduced as signal regulators in a sandwich immunoassay. The ECL quenching was achieved through the dual effects of ECL resonance energy transfer between PDA and the MOF, combined with the scavenging of hydroxyl radicals by PDA. Based on the changes in the ECL signal, an ultrasensitive determination of Cyfra 21 − 1 was realized, with a linear range from 10 fg/mL to 10 ng/mL and a detection limit as low as 2.04 fg/mL. The sensor has been successfully applied to the determination of Cyfra 21 − 1 in serum samples. Graphical
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高影响因子
JOURNAL OF FLUORESCENCE
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2026
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IF 3.4
Wang Zhihui,Wang Xiaohua,Jia Yumeng,Wang Jing,Shi Zhongxiang,Yan Qingyun
A narrow-band green-emitting phosphor KAl 11 O 17 (KAO): Eu 2+ , Mn 2+ , was synthesized via a high-temperature solid-state reaction to evaluate its potential for use in high-quality backlight displays. Structural refinement reveals that Eu 2+ and Mn 2+ ions preferentially occupy distinct crystallographic sites: Eu 2+ resides at K + sites in the conductive layer, whereas Mn 2+ substitutes for tetrahedral Al 3+ sites within the spinel block. This spatial separation facilitates efficient energy transfer (ET) from Eu 2+ to Mn 2+ . Spectroscopic analysis of the optimally doped composition, KAO: 0.07Eu 2+ , 0.04Mn 2+ , indicates that the ET proceeds predominantly via a dipole - quadrupole ( d - q ) mechanism. The resulting phosphor exhibits bright green emission centered at 510 nm with an exceptionally narrow full width at half maximum (FWHM) of 8.13 nm, a high color purity of 98%, and an internal quantum efficiency (IQE) of 65.41%. Moreover, the material demonstrates excellent thermal stability, retaining 93.11% of its initial luminescence intensity at 423 K, corresponding to a thermal activation energy of 0.2917 eV. To demonstrate its practical utility, a white LED device was fabricated by combining the optimized green phosphor (KAO: 0.07Eu 2+ , 0.04Mn 2+ ) with a blue phosphor (BaMgAl 10 O 17 (BAM): Eu 2+ ), a red phosphor (Ca 9 KMn(PO 4 ) 7 : Eu 2+ ), and a 365 nm near-ultraviolet chip. The resulting device achieves a wide color-gamut covering 107.8% of the NTSC standard. Collectively, these results demonstrate that precise control of site occupancy and energy transfer enables the design of green phosphors that simultaneously exhibit narrow-band emission, high color purity, and robust thermal stability-properties that are essential for wide color-gamut WLED backlight displays.
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高影响因子
JOURNAL OF MATERIALS SCIENCE
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2026
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IF 4.4
Li Xiaoguang,Chen Jia,Li Aoqi,Li Jing,Wang Mingyu,Li Liangsheng,Shangguan Enbo
A novel in situ self-sulfidation approach was devised to fabricate ZnO/ZnS/C ternary nanocomposites as highly stable anodes for alkaline Zn–Ni batteries. Zinc sulfate acted as a dual-purpose precursor, providing both zinc and sulfur, whereas acrylamide served as the carbon source and in situ reductant. In a single-step carbothermal pyrolysis at 800 °C, the carbon matrix converted sulfate ions to sulfide, facilitating the simultaneous generation of electrochemically active ZnO, a protective ZnS layer, and a conductive carbon network during a single thermal treatment. The optimized ZnO/ZnS/C-2 electrode exhibited a discharge capacity of 576.8 mAh g −1 after 600 cycles at 1 C and maintained 513.2 mAh g −1 at 15 C. Under identical conditions at 10C, the ZnO/ZnS/C-2 electrode delivered a capacity of 545.3 mAh g −1 , which is 41.5% higher than that of commercial ZnO (385.4 mAh g −1 ). Upon the current density reverting to 0.2 C, it regained 96.6% of its original capacity, indicating remarkable reversibility. Post-cycling scanning electron microscopy images validated the successful inhibition of zinc dendrite proliferation. The performance improvements arise from the synergistic combination of the protective ZnS layer, the interconnected conductive carbon framework, and the advantageous ZnO/ZnS heterointerface, which collectively boost structural stability and charge transfer kinetics.
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高影响因子
MICROCHIMICA ACTA
·
2026
·Vol. 193
·期 9
·635
·
IF 5.4
Wang Yu,Zhang Shumin,Shi Jiale,Wang Yuetong,Mao Yexuan,Dang Meng,Huang Xianqing,Song Lianjun,Zhang Xiya,Bu Tong
A novel fluorescent lateral flow assay (FLFA) based on a zirconium-based metal aggregation-induced emission luminogen framework (Zr-MAF) is reported for the highly sensitive detection of zearalenone (ZEN) in cereals. A carambola-like Zr-MAF with a high fluorescence quantum yield of 36.9% was synthesized via a hydrothermal method using Zr 4+ and 1,1,2,2-tetra(4-carboxylphenyl) ethylene (TCPE). The prepared Zr-MAF-labeled monoclonal antibody probe exhibited intense luminescence, robust stability, and high affinity toward ZEN, collectively contributing to a significant enhancement in detection sensitivity. Under optimal conditions, the Zr-MAF-FLFA achieved an ultralow detection limit (IC 10 = 0.014 ng/mL) and a sensitivity (IC 50 ) of 0.046 ng/mL, representing a 2.6-fold improvement over traditional gold nanoparticles-based FLFA. Notably, the assay exhibited significant cross-reactivity only with the ZEN homologues α-ZAL, β-ZAL, and β-ZOL, which shared similar electrostatic potentials and substantial 2D molecular similarities with ZEN. Furthermore, the proposed method was successfully applied to real food matrices, including flour, glutinous rice, sweet corn, and glutinous corn, yielding satisfactory recoveries ranging from 85.37% to 106.42%. With detection limits in these food samples (0.68-0.78 µg/kg) falling well below national regulatory limits, this work provides a robust analytical platform for trace mycotoxin monitoring in food safety. Graphical abstract
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高影响因子
Scientific Reports
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2026
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IF 4.9
Zhang Wei,Zhu Xinghao,Shao Mingliang,Han Qi,Shen Hao,Zhang Kun,Chen Rui,Qi Dongmei,Xu Lijun,Wu Zongyao
The progression of hepatocellular carcinoma (HCC) was highly dependent on pathological angiogenesis, with tumor-associated macrophages (TAMs) serving as key mediators regulating angiogenesis within the tumor microenvironment. The role of protein tyrosine phosphatase 2 (SHP2), a multi-signaling pathway regulator containing an SH2 domain, in TAM-mediated angiogenesis remained unclear. This study aimed to elucidate the molecular mechanism by which SHP2 regulates HCC angiogenesis through the ROS/Src pathway in TAMs under hypoxic conditions. We employed a comprehensive approach. THP-1 macrophage cells were transfected with SHP2 shRNA lentivirus and co-cultured with HCC cell line Huh-7 cells. The co-cultured cells were then subcutaneously transplanted into nude mice. Tumor size was assessed via HE staining in nude mouse tumor formation assays. We engineered luciferase-transfected Huh-7 cells to establish an orthotopic HCC implantation model and measured tumor area via in vivo fluorescence imaging. THP-1 cells were respectively cultured in media supplemented with antioxidants, pro-oxidants, and Src inhibitors, followed by transfection with SHP2 shRNA lentivirus and SHP2 mock lentivirus. These cells were then co-cultured with Huh-7 cells and Hep3B cells, respectively. The proportion of CD68-positive cells detected by immunofluorescence staining was used to ensure that the observed effects in the study were primarily derived from tumor-associated macrophages. Western blot analysis was employed to detect expression levels of SHP2, ROS/Src pathway-related proteins, tumor migration-related proteins, and angiogenesis-related proteins in the cells. Relative fluorescence intensity of intracellular ROS in THP-1 cells was visualized using the fluorescent probe DCFH-DA combined with fluorescence microscopy. Cell migration and invasion capabilities were assessed via wound healing assays and transwell assays. Immunofluorescence staining further validated SHP2 expression levels in THP-1 cells. Additionally, we examined the effects of SHP2 on HCC angiogenesis using tube formation assays, Western Blot analysis, HE staining, and immunohistochemical staining for CD31. The impact of SHP2 on HCC cell proliferation was investigated through colony formation assays and cell cycle analysis by flow cytometry. Following co-culture of SHP2 shRNA-infected THP-1 cells with Huh-7 cells, nude mouse tumor formation assays and in vivo fluorescence imaging revealed significantly reduced tumor volume and area. Following antioxidant supplementation in THP-1 cell culture medium, western blot analysis revealed markedly reduced expression levels of ROS/Src pathway-associated proteins, tumor migration proteins, and angiogenesis-related proteins. Fluorescent probe-based fluorescence microscopy demonstrated decreased relative fluorescence intensity of ROS within tumor cells. Furthermore, Western blot and immunofluorescence staining experiments jointly demonstrated that SHP2 in TAMs can regulate the ROS/Src pathway. Wound healing assays, transwell assays, and tube formation assays demonstrated that SHP2 in TAMs enhanced HCC cell migration, invasion, and angiogenesis capabilities. Furthermore, HE staining and immunohistochemical staining for CD31 indicated that inhibiting ROS/Src pathway suppressed HCC angiogenesis. Colony formation assay and flow cytometry analysis revealed that SHP2 in TAMs promotes HCC proliferation and cell cycle progression via the ROS/Src pathway. Under hypoxic conditions, tyrosine phosphatase SHP2 in TAMs regulates angiogenesis in HCC through the modulation of the ROS/Src pathway.
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PubMed
高影响因子
CATALYSIS LETTERS
·
2026
·Vol. 156
·期 7
·205
·
IF 2.5
Zhang Yikang,Zhang Yihu,Sun Min,Li Bin,Wang Haiyan,Li Zijiong
The oxygen reduction reaction (ORR) serves as the core cathodic reaction for fuel cells. However, the sluggish ORR kinetics and high cost of Pt-based catalysts severely restrict the commercialization of fuel cell devices. Herein, a facile in-situ synthetic strategy is developed to fabricate carbon dot-supported cobalt (CD@Co) electrocatalysts, in which carbon dots (CDs) act as both reducing agent and structural modulator. With the aim of optimizing catalytic activity and stability, the effects of CDs dosage on Co dispersion, nitrogen configuration and ORR performance are systematically investigated. The optimized CD@Co-0.12 exhibits a half-wave potential of 0.89 V (vs. RHE) and a limiting current density of 4.47 mA·cm − 2 , outperforming commercial 20% Pt/C (E 1/2 = 0.85 V). Kinetic analysis reveals a Tafel slope of 90.65 mV·dec − 1 and a near-four-electron transfer pathway ( n ≈ 3.78). After 5000 CV cycles, only negligible potential decay is observed, demonstrating excellent stability. This work provides a low-cost and scalable strategy for designing high-performance non-precious metal ORR catalysts. Graphical Carbon dot regulated CD@Co non-precious electrocatalyst toward efficient alkaline oxygen reduction reaction
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高影响因子
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