CARDIOVASCULAR DRUGS AND THERAPY
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2025
·
IF 3.1
Ba Lina,Wu Nan,Feng Xiang,Wang Ruixuan,Zhao Zhichao,Wang Rui,Liu Renling,Shi Pilong,Sun Hongli,Qi Hanping
Purpose The purpose of this study was to investigate the protective effects of biochanin A (BCA) on cardiac hypertrophy and to elucidate the underlying molecular mechanisms. The research question was whether BCA can reverse heart dysfunction and attenuate cardiomyocyte hypertrophy induced by pressure overload and AngII, respectively, and how it interacts with the NLRP3 pyroptosis pathway to achieve these effects. Methods We employed an animal model of pressure overload-induced cardiac hypertrophy and an in vitro model of AngII-induced cardiomyocyte hypertrophy to assess the effects of BCA. The expression of NLRP3 and its related signaling molecules was analyzed by western blotting, and the activity of the NLRP3 pathway was measured using pyroptosis assays. The role of Cbl-b, an E3 ubiquitin ligase, in BCA-mediated NLRP3 inhibition was also investigated. Results BCA was found to reverse heart dysfunction and attenuate cardiomyocyte hypertrophy induced by pressure overload and AngII. Mechanistically, BCA mitigated cardiac hypertrophy by targeting the NLRP3 pyroptosis pathway. The reduction in NLRP3 expression by BCA was predominantly mediated through the upregulation of Cbl-b, which enhanced the ubiquitination and subsequent degradation of NLRP3. Additionally, BCA facilitated the upregulation of Cbl-b expression by interacting with NF-κB, preventing NF-κB binding to the promoter region of Cbl-b and reversing its suppressive action on Cbl-b expression. Conclusion This study provides initial evidence that BCA can protect against cardiac hypertrophy. Its mechanism of action involves interacting with NF-κB to promote the expression of Cbl-b, which facilitates the ubiquitination and degradation of NLRP3, ultimately inhibiting pyroptosis. This finding suggests that BCA may be a potential therapeutic agent for the treatment of cardiac hypertrophy.
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INTERNATIONAL IMMUNOPHARMACOLOGY
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2024
·
IF 4.8
Bo Wang,Jiquan Shen,Xinggao Wang,Ruixing Hou
Previous study has indicated that Celastrol (Cel) has various physiological and pharmacological effects, including antibacterial, antioxidant, pro-apoptotic, anticancer and anti-rheumatoid arthritis (RA) effects. However, low water solubility, low oral bioavailability, narrow treatment window, and high incidence of systemic adverse reactions still limit the further clinical application of Cel. Here, aiming at effectively overcome those shortcomings of Cel to boost its beneficial effects for treating RA, we developed the leukosome (LEUKO) coated biomimetic nanoparticles (NPs) for the targeted delivery of Cel to arthritis injury area in RA. LEUKO were synthesized using membrane proteins purified from activated J774 macrophage. LEUKO and Cel-loaded LEUKO (Cel@LEUKO) were characterized using dynamic light scattering and transmission electron microscopy. Our results demonstrated that Cel@LEUKO can inhibit the inflammatory response of lipopolysaccharide (LPS) induced mouse monocyte macrophage leukemia cells (RAW264.7 cells) and human rheumatoid arthritis synovial fibroblasts (MH7A) cells through the inhibition of reactive oxygen species (ROS)-NF-κB pathway. In addition, research has shown that LEUKO effectively targets and transports Cel to the inflammatory site of RA, increased drug concentration in affected areas, reduced systemic toxicity of Cel, and reduced clinical symptoms, inflammatory infiltration, bone erosion, and serum inflammatory factors in collagen-induced arthritis (CIA) rats.
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DALTON TRANSACTIONS
·
2024
·Vol. 54
·期 1
·144-151
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IF 3.5
Yuan Rui,Zong Li,Miaohui Wang,Yunxia Liu,Haiping Lin,Peipei Huang,Qing Li
Developing electrocatalysts with fast reaction kinetics for the urea oxidation reaction (UOR) in the field of sustainable hydrogen production through urea-assisted water splitting remains challenging. Here, Ni1−xO/Ni(OH)2 supported on nickel foam (Ni1−xO/Ni(OH)2/NF) is prepared via a defect engineering strategy by combining Zn doping and acid etching. The doped Zn species are partially removed, facilitating the formation of NiOOH during acid etching. Residual Zn species modulate the electronic structure of nickel sites, which intrinsically accelerate the reaction kinetics of Ni1−xO/Ni(OH)2/NF. Ni1−xO/Ni(OH)2/NF exhibits excellent performance for the UOR with a low potential of 1.346 V versus the reversible hydrogen electrode to attain 100 mA cm−2, fast reaction kinetics (18.7 mV dec−1), and excellent stability in an alkaline electrolyte. The enhanced reaction kinetics of Ni1−xO/Ni(OH)2/NF are clearly elucidated by operando electrochemical impedance spectroscopy and in situ Raman spectroscopy. Our study offers an effective approach for designing promising Ni-based UOR catalysts for the practical application of urea-assisted water splitting.
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FOOD CHEMISTRY
·
2025
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IF 9.8
Yudie Sun,Kehong Quan,Ruilai Zhang,Aobo Feng,Mingfu Ye,Kui Zhang
Methicillin-resistant Staphylococcus aureus (MRSA) is a ubiquitous foodborne pathogen capable of causing food poisoning and producing enterotoxins in foodstuffs, which ultimately results in various illnesses, such as vomiting, diarrhea, and pneumonia. In this study, we present a MoS 2 NF@AuNPs enhanced electrochemiluminescence (ECL) biosensor for MRSA detection based on a DNA branching tree structure formed via enzyme-free hybridization chain reaction (HCR) amplification. This approach integrates bacterial aptamers with multistage HCR amplification to achieve highly sensitive and specific target recognition. Furthermore, MoS 2 NF@AuNPs act as a synergistic catalyst for Ru(bpy) 3 2+ molecules, which in turn substantially enhances the signal readout of the biosensor. The biosensor exhibits a robust linear correlation for MRSA detection over a concentration range of 10 0 to 10 7 cfu/mL, with a detection limit of 1 cfu/mL. In addition, the biosensor demonstrates excellent selectivity and high sensitivity when applied to real samples such as water, juice, and milk.
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Catalysts
·
2025
·Vol. 15
·期 3
·285
·
IF 4
Sirong Li,Lang Yao,Zhenlong Wang,Zhonghe Xu,Xuechun Xiao
In this study, a sulfur-doped cobalt–iron catalyst (CoFeS/NF) was synthesized on a nickel foam (NF) substrate via a facile one-step electrodeposition method, and its performance in urea electrolysis for hydrogen production was systematically investigated. Sulfur doping induced significant morphology optimization, forming a highly dispersed nanosheet structure, which enhanced the specific surface area increase by 1.9 times compared with the undoped sample, exposing abundant active sites. Meanwhile, the introduction of sulfur facilitated electron redistribution at the surface modulated the valence states of nickel and cobalt, promoted the formation of high-valence Ni3+/Co3+, optimized the adsorption energy of the reaction intermediates, and reduced the charge transfer resistance. Electrochemical evaluations revealed that CoFeS/NF achieves a current density of 10 mA cm−2at a remarkably low potential of 1.18 V for the urea oxidation reaction (UOR), outperforming both the undoped catalyst (1.24 V) and commercial RuO2(1.35 V). In addition, the catalyst also exhibited excellent catalytic activity and long-term stability in the total urea decomposition process, which was attributed to the amorphous structure and the synergistic enhancement of corrosion resistance by sulfur doping. This study provides a new idea for the application of sulfur doping strategy in the design of multifunctional electrocatalysts, which promotes the coupled development of urea wastewater treatment and efficient hydrogen production technology.
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Translational Andrology and Urology
·
2024
·Vol. 13
·期 9
·1971
·
IF 1.9
Jiahao Jiang,Fei Xiao,Lanxin Yang,Yan Zeng,Jing Chen,Hengcheng Zhu,Lingqi Liu
Background Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common male urological disease characterized by chronic pelvic pain and various discomforts. Astaxanthin (AST) has multiple functions, including anti-inflammatory property, but it is unclear whether AST plays a key role in CP/CPPS and how it works. This study aimed to investigate the protective effect of AST on CP/CPPS in rats and the underlying mechanism. Methods A CP/CPPS rat model was induced by intraprostatic injection of carrageenan and the blood specimens and prostates were harvested for further research after oral administration of AST for 4 weeks. Results Tactile allodynia test showed that AST ameliorated chronic pelvic pain in a dose-depended manner. In addition, histological evaluation indicated that AST alleviated CP/CPPS rat prostate histological inflammation. Meanwhile, AST suppressed the expression of proinflammatory cytokines, including interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor-α (TNF-α). Besides, AST inhibited the activities of prostaglandin E2 (PGE2) and cyclooxygenase 2 (COX2). Furthermore, AST decreased the activation of the nuclear factor-κB (NF-κB) signaling pathway. Conclusions Our study has shown that AST exerts an anti-inflammatory and protective effect against CP/CPPS and the function is mediated at least through the suppression of NF-κB signaling pathway. These results provide evidence of AST as the potential agents for the treatment of CP/CPPS.
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Journal of Inflammation Research
·
2025
·
IF 4.1
Zhongzhu Ai,Dongfeng Yuan,Yun Li,Jingyi Cai,Daonian Zhou,Wei Liu
Background Hemorrhoidal disease (HD) is characterized by the pathological dilation of anal vascular cushions, causing pain, itching and bleeding. Recent evidence links HD onset and progression to rectal inflammation. Medical Hemorrhoid Gel (MHG), a multi-component botanical preparation, has gained empirical validation for HD management. This study aims to systematically evaluate the safety, efficacy, and mechanism of action of MHG in treating HD.Methods The phytochemical composition of MHG was characterized using UPLC-QTOF-MS/MS and GC-MS/MS analyses. In vivo, the efficacy was assessed in a croton oil preparation (COP)‑induced HD rat model (n=10 per group) via anorectal coefficient (ARC) measurement, macroscopic severity score, Evans blue extravasation quantification, and H&E/PAS staining. Transcriptomic sequencing of anorectal tissues was integrated with experimental validation using ELISA, immunohistochemistry (IHC), and Western blotting to delineate molecular mechanism. Data were analyzed by one-way analysis of variance (ANOVA) followed by Dunnett’s multiple comparison post hoc test (significance at p<0.05).Results MHG significantly reduced ARC, macroscopic severity score, and Evans blue extravasation, restored intestinal villus structure and goblet cell numbers, and alleviated inflammation. Acute toxicity tests showed that MHG did not cause anorectal abnormalities or systemic toxicity in rats. Transcriptomic analysis integrated with experimental validation suggested the therapeutic mechanism of MHG involves inflammation response and NF-κB pathway. Specifically, MHG suppressed the levels of the pro-inflammatory mediator TNF-α, while it enhanced the levels of the anti-inflammatory mediator IL-10. Mechanistic studies revealed that MHG inhibited NLRP3 inflammasome activation, reduced the phosphorylation level of p65 and enhanced IκBα expression. Phytochemical analysis identified 20 constituents that contribute to the bioactivity of MHG.Conclusion Our study substantiated that MHG exerts anti-hemorrhoidal effects through NLRP3 inflammasome suppression via NF-κB pathway regulation. This mechanistic insight provides scientific validation for clinical application of MHG in HD management.
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JOURNAL OF PHARMACOLOGICAL SCIENCES
·
2025
·
IF 2.9
Jingwei Liu,Cheng Qiu,Xiaoxiong Wang,Ziqian Xiang,Junyuan Sun,Mingzheng Chang,Qingliang Ma,Yan Zhuang,Yunpeng Zhao,Qiang Yang,Lianlei Wang,Xinyu Liu
Fracture is a common type of traumas and alternative therapies to boost bone fracture healing is necessary. The aim of this study is to elucidate the role of sulfasalazine in bone fracture healing by using MC3T3-E1 cells in vitro and murine femoral fracture model in vivo . Western blotting, flow cytometry, RNA sequencing, Calcein AM/PI staining, Alizarin-Red-S staining, ALP activity assay, transmission electron microscope, histological staining, immunohistochemistry, immunofluorescence and Surface plasmon resonance analysis were performed in this study. Sulfasalazine failed to elicit ferroptosis in osteoblasts within acceptable dose manner while promoted osteogenic differentiation. Furthermore, sulfasalazine was identified to inhibit inflammation by declination of inflammatory biomarkers. Besides, TNFα was verified as a potential downstream target for sulfasalazine and the adverse effect of TNFα on osteogenic differentiation could be largely salvaged by sulfasalazine due to direct binding between these two molecules. RNA-seq further implied decreased transcription of genes related to NF-κB pathway. Murine study showed sulfasalazine promotes fracture healing as evidenced by increased bone remodeling both histologically and radiologically. Overall, sulfasalazine accelerates osteogenic differentiation and promotes bone healing by direct binding to and thus inhibiting TNFα, which subsequently suppresses NF-κB signaling. Therefore, sulfasalazine shows a promising outcome for the treatment of bone fracture.
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NEW JOURNAL OF CHEMISTRY
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2024
·Vol. 48
·期 41
·17990-17997
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IF 2.7
Biaobiao Lu,Yaoxia Yang,Yu Zhang,RuiRui Zhang,Fuxing Zhou,Qingtao Wang,Wei Zeng,Dongfei Sun
The exploration of clean, environmentally friendly, efficient and economical metal electrocatalysts is becoming more and more in-depth, but catalyst activity and stability are still the main goals. Herein, a thin regular pentagonal rough nanosheet array (La-CoNiOOH@FeSe@NiSe/NF) grown on a three-dimensional porous conductive surface was designed and synthesized. The prepared electrode material exhibited good catalytic activity in 1 M KOH solution, required only 270 mV of overpotential to provide 10 mA cm−2 current density for the oxygen evolution reaction (OER), and showed excellent stability for at least 90 hours during the OER process. The characterization test results proved that the incorporation of La changed the surface electronic structure, optimized the interface, modulated the active site on the surface of the material, and exposed a large number of active sites, thus improving the activity and stability of the catalyst material. At the same time, such a rough surface also gives the material excellent wettability and anti-bubble adhesion, which is also a key factor in maintaining the catalytic activity and OER stability of the material. This method provides a new idea for developing an efficient and economical electrolytic hydroelectricity catalyst.
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BMC Nephrology
·
2025
·Vol. 26
·期 1
·1-14
·
IF 2.4
Lou Yunpeng,Shi Hongguang,Sha Ning,Li Feifei,Gu Xiaofeng,Lin Huiyan
Background Ursodeoxycholic acid (UDCA), traditionally recognized for its hepatoprotective effects, has also shown potential in protecting kidney injury. This study aimed to evaluate the protective effects of UDCA against sepsis-induced acute kidney injury (AKI) and to elucidate the underlying mechanisms.Methods Sixty male C57BL/6 N mice were utilized to establish a sepsis-induced AKI model through intravenous injection of lipopolysaccharides (LPS, 10 mg/kg). UDCA (15, 30, and 60 mg/kg) was administered intraperitoneally once daily for 7 days before LPS injection. Kidney injury was evaluated by HE staining and biochemical markers, including serum creatinine (Cr), blood urea nitrogen (BUN), urinary protein, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and retinol binding protein (RBP). Oxidative stress parameters and nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) pathway, pro-inflammatory cytokines and nuclear factor-kappa B (NF-κB) pathway were also evaluated. Additionally, HK-2 cells were treated with LPS in vitro, and cell viability and apoptosis were detected using CCK-8 kit and flow cytometer, respectively.Results UDCA significantly attenuated LPS-induced renal histopathological damage and improved renal function, as evidenced by reduction in serum Cr, BUN, and urinary protein levels. UDCA also up-regulated the protein expression of zonula occludens-1 (ZO-1) and Ezrin in the kidney, and reduced the urinary levels of NGAL, KIM-1, NAG, and RBP. Moreover, UDCA inhibited NF-κB p65 phosphorylation and reduced pro-inflammatory cytokines levels (TNF-α, IL-1β, and IL-6) in both serum and kidney. UDCA alleviated oxidative stress by activating the Nrf2/HO-1 pathway in the kidney. In vitro, UDCA reduced LPS-induced cell injury and apoptosis in HK-2 cells, with these protective effects being blocked by the Nrf2 inhibitor ML385.Conclusion sOur present study demonstrated that UDCA exerts protective effects against sepsis-induced AKI by attenuating oxidative stress and inflammation, primarily through the activation of the Nrf2/HO-1 pathway and inhibition of the NF-κB pathway. These findings highlight the therapeutic potential of UDCA in preventing sepsis-induced AKI.
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ONCOLOGY REPORTS
·
2025
·Vol. 54
·期 6
·1-14
·
IF 3.9
Wei-Wei Zheng,Jia-Xuan Ding,Yang-Xin Liang,Ling Ye
Thymoquinone (TQ) is a quinone isolated from the black seed Nigella sativa and has been extensively investigated in the pharmaceutical field due to its promising therapeutic value. There have been reports on the potential anti‑cancer properties of TQ, whereas the clinical application of TQ is greatly restricted by its low water solubility and poor delivery. In the present study, TQ was encapsulated into hydroxypropyl‑β‑cyclodextrin (HP‑β‑CD) using the freeze‑drying method to form a TQ/HP‑β‑CD inclusion complex. Then, the TQ/HP‑β‑CD inclusion complex was characterized by Fourier transform infrared, differential scanning calorimetry, X‑ray diffraction and scanning electron microscopy. HP‑β‑CD as an excipient significantly enhances the water solubility of TQ, and TQ/HP‑β‑CD demonstrated excellent biocompatibility on normal cells both in vitro and in vivo. Moreover, the complexation with HP‑β‑CD enhanced the anticancer activity of TQ against non‑small cell lung cancer cells and its mechanism of action is related to ferroptosis mediated by NF‑κB. Such an enhanced cytotoxic effect may be attributed to the effective complexation of TQ in HP‑β‑CD, which enhances its water solubility and bioavailability.
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MICROBIAL PATHOGENESIS
·
2025
·
IF 3.5
Kai Liu,Hong Sun,Hong Wang,Junbo Zheng,Xiuzhen Wang,Xin Wang,Yeting Hou,Qian Ye,Ji Li
Sepsis is a systemic inflammatory response syndrome triggered by infection. Severe sepsis is associated with dysbiosis of the intestinal flora and impaired intestinal function. Ellagic acid (EA) is a natural compound known for its ability to inhibit bacteria and viruses, thereby preventing infections. However, it remains unclear whether EA mitigates intestinal barrier dysfunction. In this work, BALB/c mice were administered doses of EA via gavage, followed by an injection of lipopolysaccharide (LPS) to induce sepsis. Fecal samples, serum, and ileum tissues were collected for molecular or pathological analysis. The intestinal contents underwent 16S rRNA sequencing and targeted metabolomics for short-chain fatty acids (SCFAs) detection. Additionally, an in vitro injury model was established using IEC6 cells treated with LPS; subsequent changes in inflammation and oxidative stress were assessed following EA treatment. The results indicated that EA reduced inflammation and oxidative stress as well as ameliorated intestinal lesions and enhanced intestinal barrier function in both mouse and cell models. Moreover, EA inhibited the signaling of nuclear factor kappa-light-chain-enhancer of activated B cells/myosin light chain kinase/myosin light chain (NF-κB/MLCK/MLC) pathway. Besides, EA also rectified genomic and metabolomic disturbances within the gut microbiota caused by sepsis. In conclusion, EA mitigates sepsis-induced intestinal injury through modulation of gut microbiota composition and inhibition of NF-κB-mediated MLCK/MLC signaling pathway. Thus, EA might represent a promising therapeutic agent for addressing intestinal injuries associated with sepsis.
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