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Frontiers in Nutrition · 2026 · IF 5.5

Pachymic acid alleviates hepatic lipid accumulation and oxidative stress in MASLD via regulation of the Keap1–Nrf2–HO-1 signaling axis

Maoru Li,Zefeng Wang,Huan Zhai,Jiajiao Li,Ji Ma,Bin Qiu

BackgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a rapidly growing metabolic disorder with no FDA-approved treatment. Pachymic acid (PA; synonym: 3-O-acetyltumulosic acid), a lanostane-type triterpenoid, shows potential for treating MASLD. However, its mechanisms remain underexplored.ObjectiveThis work evaluated the therapeutic efficacy and mechanisms of PA in treating MASLD.MethodsThe high-cholesterol diet (HCD)-induced zebrafish model, high-fat diet induced C57BL/6 mice model and free fatty acid (FFA)-treated BRL-3A cells was used to assess PA’s anti- MASLD effects in vivo and in vitro.ResultsPA improved lipid metabolism disrupted by HCD, reduced hepatic oxidative stress, as indicated by decreased MDA levels and increased SOD activity, and lowered inflammatory markers, including TNF-α, IL-6, and IL-1β. PA also enhanced antioxidant activity by regulating the Keap1-Nrf2-HO-1 pathway. PA decreased Keap1 mRNA expression induced by reactive oxygen species (ROS), upregulated Nrf2 and HO-1 expression, and promoted Nrf2 nuclear translocation. These effects suggest that PA inhibits ROS production by activating the Keap1-Nrf2-HO-1 pathway and possibly by inhibiting Nrf2 degradation.ConclusionPA improves MASLD through lipid metabolism regulation and antioxidant effects, primarily by activating the Keap1-Nrf2-HO-1 pathway. These findings highlight PA’s potential as a therapeutic agent for MASLD.

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PROCESS BIOCHEMISTRY · 2026 · IF 4.4

An engineered suicide vector-mediated genome editing of Mycobacterium sp. LY-1 for targeted 9α-hydroxyandrost-4-ene-3,17-dione biosynthesis

Liyang Xu,Yujia Wang,Feiyu Yan,Wenjing Pan,Yingjia Tong,Jinsong Gong,Xiaomei Zhang,Jinsong Shi,Zhenghong Xu,Hui Li

Mycolicibacterium is a crucial industrial host for steroid biotransformation, yet its genetic engineering has long been limited by inefficient homologous recombination (HR) and strong non-homologous end joining (NHEJ) activity. Here, we established and optimized a suicide plasmid-based genome editing system for Mycobacterium sp. LY-1. The constructed vector p2NILB, combining kanamycin selection with sacB-mediated counter-selection, enabled precise and markerless allelic exchange. Suppression of NHEJ through deletion of ku or ligD , together with optimization of homology arm length, increased gene knockout efficiency to over 70%. This optimized platform was subsequently applied to metabolic engineering of sterol degradation to enhance 9α-hydroxyandrostenedione (9α-OH-AD) biosynthesis. Sequential deletion of five kstD isoenzymes blocked downstream steroid degradation, with kstD1 identified as the major contributor to product loss. Functional analysis revealed KshA2 as the key 9α-hydroxylase, and its overexpression increased the 9α-OH-AD titer to 3.41 g/L. In addition, deletion of the branched-chain acid transporter gene mmpL3 further enhanced 9α-OH-AD production to 4.19 g/L. To overcome substrate utilization limitations under high phytosterol loading conditions, a soybean oil‑Tween 80 solvent system overcame substrate limitation, enabling 15.71 g/L 9α‑OH‑AD from 30 g/L phytosterols. This study provides a robust genome editing framework and an effective strategy for engineering steroid-producing actinobacteria.

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JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY · 2026 · IF 5.3

Conformationally constrained 6‑aryl‑1‑(3,4,5‑trimethoxyphenyl)-1H-pyrazolo[3,4‑b]pyrazines as novel microtubule destabilizers: design, synthesis, and antitumor evaluation

Zhu Guo,Yujing Zhang,Ping Zou,Caiyun Sun,Liya Cui,Gang Wang,Chao Wang

A novel class of 6-aryl-1-(3,4,5-trimethoxyphenyl)-1H-pyrazolo[3,4-b]pyrazine derivatives was designed and synthesized as tubulin polymerization disruptors. Among them, compound 10t emerged as the most potent agent, exhibiting IC₅。 values of 0.13-0.18 µM against HeLa, SGC‑7901, and MCF‑7 cancer cell lines. Functional studies revealed that 10t effectively inhibits tubulin assembly in vitro, destabilizes cellular microtubule networks, induces G₂/M cell‑cycle arrest, and triggers apoptosis. Molecular docking indicated that 10t binds to the colchicine site on tubulin, forming a unique hydrogen bond with β‑Asn349 that is not observed with the reference compound CA‑4. Importantly, 10t showed significantly lower cytotoxicity toward normal HUVECs than CA‑4, suggesting an improved safety profile. Collectively, these findings establish the pyrazolo[3,4‑b]pyrazine scaffold as a promising platform for microtubule‑targeting anticancer agents and identify 10t as a compelling lead for further development.

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SOLAR ENERGY MATERIALS AND SOLAR CELLS · 2025 · IF 6.3

Quantitative study of hot carriers thermalization mechanisms in GAx[Cs0.05(FA0.23MA0.77)0.95]1-xPbIBr2 for hot carrier multi-junction solar cells

Yi Zhang,Huilong Chen,Junfeng Qu,Rui Wang,Shuhong Xu,Jiayu Zhang,Gavin Conibeer

The hot carrier multi-junction solar cell (HCMJSC) is an advanced concept solar cell with a theoretical efficiency greater than 65 %, which consists of a thin top junction with a wide bandgap and a thick bottom junction with a narrow bandgap to absorb high and low energy photons, respectively. Wide bandgap perovskites are expected to be a suitable candidate for top absorption layers due to their ease of band engineering. However, the carrier thermalization mechanisms of quaternary A-site perovskites have not been well studied until now. Conventionally, the incorporation of larger A-site cations induces lattice expansion and enhances thermal fluctuations, thereby accelerating carrier cooling. In this work, the incorporation of guanidinium (GA) did not immediately shorten the cooling process but instead exhibited a non-monotonic trend, initially slowing then accelerating the thermalization process. The thermalization coefficients ( Q th ) of the quaternary A-site perovskites with different GA doping ratio were obtained from the power dependent-steady state photoluminescence spectra. Moderate addition of GA can prolong the thermalization process of the hot carriers and reduce Q th , which will improve power conversion efficiency, with the optimal effect achieved at 3 % GA incorporation in the A-site. This work lays the foundation for a theoretical framework that incorporates perovskite materials which may be suitable as the top absorption layer of HCMJSC.

CAS / MDL: 10031-22-8 10101-63-0
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Journal of Environmental Sciences · 2025 · IF 6.3

Multifunctional assays and molecular simulations reveal the protective mechanisms of QNZ in mitigating PFOA-Induced cytotoxicity in Nthy-ori3-1 cells

Xiaotian Huang,Zuhong Lin,Denglong Lu,Haipu Li

Perfluorooctanoic acid (PFOA) is a persistent toxic chemical that enters the human body through the food chain and causes harm. In this study, human thyroid follicular epithelial cells (Nthy-ori3-1 cells) were used as a model. PFOA was shown to reduce cell viability through a cell activity assay. Notably, at a concentration of 100 μmol/L, PFOA enhanced the activity of antioxidant enzymes ((Total superoxide dismutase (T-SOD), catalase (CAT), glutathione (GSH), total Antioxidant Capacity (T-AOC)), while the level of intracellular reactive oxygen species (ROS) remained elevated. PFOA triggered oxidative stress by inducing abnormal ROS levels, which subsequently exacerbated the inflammatory response and affected cellular activity. Therefore, pretreatment with 10μmol/L EVP4593 (QNZ, an NF-κB inhibitor) increased the percentage of normal cells from 74.06 % to 83.74 % at 1 μmol/L PFOA. Molecular docking and molecular dynamics indicated that QNZ competitively inhibited the interaction between PFOA and nuclear factor kappa-B (NF-κB) proteins. Correspondingly, Western blotting and qPCR analyses confirmed that QNZ suppressed the expression of apoptosis-related proteins ((Tumor protein p53 (P53), tumor necrosis factor-alpha (TNF-α), Bcl2-associated X (BAX), B-cell lymphoma-2 (BCL-2), cysteine aspartate protease-3 (Caspase-3), NF-κB) and their related genes. Additionally, PFOA prompted cells to release T4 and T3. This study not only elucidates the toxic effects of PFOA on cells, but also reveals the defense mechanism by which QNZ effectively alleviates cell toxicity.

CAS / MDL: 67-68-5
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Biomedical Materials · 2024 ·Vol. 19 ·期 3 ·035011 · IF 3.9

Synthesis and characterization of 3-in-1 multifunctional lipiodol-doped Fe3O4@Poly (diallyl isophthalate) microspheres for arterial embolization, chemotherapy, and imaging

Piaoyi Chen,Qinglin Xiao,Zhaoxiong Guo,Wei Liang,Ou Liu,Liteng Lin,Yugang Huang,Kangshun Zhu,Guodong Ye

Transcatheter arterial embolization plays a pivotal role in treating various diseases. However, the efficacy of embolization therapy in cancer treatment can be limited by several factors, such as inevitable incomplete or non-target embolization, and the tumor recurrence and metastasis caused by the hypoxic microenvironment. Moreover, it is essential to explore simpler, more economical, and efficient methods for microsphere synthesis. Herein, we achieved one-step photocatalytic synthesis of lipiodol-doped Fe3O4@Poly (diallyl iso-phthalate) multifunctional microspheres (IFeD MS) for arterial embolization, chemotherapy, and imaging. The prepared microspheres are in the shape of dried plums, with a particle size of 100–300 μm. Lipiodol demonstrates a certain degree of chemotherapeutic activity, and the incorporation of Fe3O4 enables the microspheres to exhibit magnetothermal response and magnetic resonance imaging capabilities. Furthermore, the radiopaque characteristics of both agents provide the microspheres with promising potential for computed tomography and digital radiography imaging. The renal embolization experiment in rabbits demonstrated that IFeD MS achieved significant embolization and chemotherapeutic effects. Biocompatibility experiments revealed that this embolic agent did not induce tissue damage or inflammation beyond the treatment area. Additionally, IFeD MS exhibited promising imaging potential. The results of this study imply that the developed multifunctional embolic agent IFeD MS may have significant potential in transforming tumors previously only suitable for palliative cares into resectable radical treatments.

CAS / MDL: 9002-89-5
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CELLULAR SIGNALLING · 2025 · IF 3.7

Roflumilast inhibits neuronal ferroptosis via AMPK/Nrf2/HO-1 signaling and promotes motor function recovery after spinal cord injury in rats

YaoNan Han,XingTong Wang,DeShui Yu

Spinal cord injury (SCI) is a serious central nervous system disease. Ferroptosis is one of the major causes of spinal cord neurological loss, and targeting ferroptosis is a promising therapeutic strategy. Roflumilast has shown promising applications in the treatment of neurological diseases due to its potent anti-inflammatory and anti-oxidative stress effects. This study aimed to investigate whether roflumilast could inhibit neuronal ferroptosis to improve motor function after SCI in rats. In vitro experiments, we found that roflumilast significantly increased cell survival in an in vitro ferroptosis model, improved mitochondrial function, reduced intracellular iron, reactive oxygen species (ROS), and lipid peroxides accumulation as well as the expression of the pro-ferroptosis proteins, long-chain acyl-coenzyme A synthase 4 (ACSL4), and prostaglandin-endoperoxide synthase 2 (PTGS2), and increased the expression of ferroptosis-inhibitory protein glutathione peroxidase 4 (GPX4), and ferritin heavy chain 1 (FTH1) expression. Mechanistically, these protective effects were achieved by activating AMP-dependent protein kinase (AMPK)/nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling and were attenuated when AMPK signaling was blocked. In vivo experiments, roflumilast attenuated spinal cord tissue damage, increased the number of motor neuron survivors, and improved motor function after SCI in rats. Overall, activation of AMPK/Nrf2/HO-1 signaling by roflumilast attenuated neuronal ferroptosis and improved motor function after SCI in rats.

CAS / MDL: 866405-64-3
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ANNALS OF MICROBIOLOGY · 2026 ·Vol. 76 ·期 1 ·12 · IF 3.4

Phytochemical characterization of Paenarthrobacter nicotinovorans YYH-1 from Epimedium rhizosphere and its antioxidant-mediated in vitro activity against premature ovarian failure

Li Haodong,Tao Xian,Zhang Hongji,Zhang Yafei,Liang Qiancheng,Liu Qing,Luo Lan,Wang Yan,Yang Juan,Yang Xiaosheng,Peng Mei,Li Liangqun

Purpose The aim of this study was to isolate and identify a nicotine-degrading Paenarthrobacter nicotinovorans strain from the Epimedium rhizosphere , characterize its secondary metabolites, and evaluate its potential antioxidant activity against premature ovarian failure (POF). By exploring the bioactive properties of this rhizosphere microorganism, the research sought to uncover new insights into the functional roles of plant-associated microbes and discover potential natural agents for treating oxidative stress-related diseases. Methods A strain designated YYH-1 was isolated from the E. rhizosphere and identified through morphological observations and 16S rRNA gene sequencing. Ultra-performance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS) combined with GNPS molecular networking was employed to profile the chemical components of the ethyl acetate extract from YYH-1 fermentation broth. In vitro experiments utilized the human ovarian granulosa cell line (KGN) to assess the extract’s effect on D-galactose-induced cellular senescence, measuring the activity of superoxide dismutase (SOD) as an indicator of antioxidant capacity. Additionally, molecular docking was performed to elucidate the interaction mechanisms between key compounds and the Nrf2 signaling pathway. Results The isolate was confirmed as P. nicotinovorans YYH-1. Chemical profiling identified 21 secondary metabolites, including flavonoids, phenylpropanoids, alkaloids, fatty acids, and amino acid derivatives. In vitro studies demonstrated that the YYH-1 extract significantly mitigated D-galactose-induced cellular senescence in KGN cells and effectively upregulated superoxide dismutase (SOD) activity, which increased by 50.94%, 48.27%, and 38.01% respectively compared with that in the Model group.. Molecular docking analysis revealed that 8-prenylnaringenin, a major compound in the extract, could activate the Nrf2 signaling pathway by stably binding to Keap1 and Nrf2 receptors. Conclusion This study represents the first report of P. nicotinovorans in the E. rhizosphere . The strain exhibits the potential to produce diverse bioactive secondary metabolites, and its extract demonstrates antioxidant activity against POF through the activation of the Nrf2 pathway. These findings expand our understanding of rhizosphere microbial functions and provide a basis for the development of natural anti-aging therapies targeting oxidative stress-related disorders.

CAS / MDL: 328-50-7
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RSC Advances · 2019 ·Vol. 9 ·期 15 ·8315-8325 · IF 3.049

Enhancement of neural stem cell survival, proliferation and differentiation by IGF-1 delivery in graphene oxide-incorporated PLGA electrospun nanofibrous mats

Zhiping Qi,Wenlai Guo,Shuang Zheng,Chuan Fu,Yue Ma,Su Pan,Qinyi Liu,Xiaoyu Yang

The mammalian central nervous system has a limited ability for self-repair under injury conditions. The treatment of nerve injuries has been revolutionised with the development of tissue engineering techniques. However, the lack of bioactivity has severely restricted the application of biodegradable implants for neurogenesis. Therefore, surface modification of biomaterials is crucial to improve their bioactivity and promote endogenous repair mechanisms for nerve regeneration. Insulin-like growth factor 1 (IGF-1) is a growth factor for neuroprotection and neurogenesis. In this study, IGF-1 was successfully immobilised on graphene oxide (GO)-incorporated poly(lactic-co-glycolic acid) (PLGA) biodegradable electrospun nanofibres. For the in vitro investigation, neural stem cells (NSCs) were cultured on different nanofibres to observe various cellular activities. GO enhanced NSC survival under H2O2 pre-treatment and neuronal differentiation to some extent. More importantly, the immobilisation of IGF-1 onto the PLGA/GO nanofibres resulted in significantly increased NSC survival, proliferation, and differentiation. Findings from this study revealed that using PLGA/GO electrospun nanofibres to immobilise IGF-1 has excellent potential for the enhancement of the neuroprotective and neurogenic effects of nerve implants.

✓ 已验证 DOI PubMed 高影响因子
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS · 2026 · IF 5.4

Selective depression of pyrite by 3-mercapto-1-propanol in Ni-Co sulfide flotation: A mechanistic study based on surface chemisorption

Renfan Chen,Kaile Zhao,Weilong Wu,Kunxi Huang,Mengyao Zhou,Xiaolong Huang,Bing Deng,Zhen Wang,Wenpu Zhang

Efficient flotation separation of pentlandite from pyrite is central to improving the utilization efficiency of nickel-cobalt sulfide resources. In this work, 3-mercapto-1-propanol (3-MP) was employed as a selective pyrite depressant in Ni-Co sulfide flotation. The selective depression mechanism was elucidated through single-mineral, artificial mixed-mineral and real ore flotation tests, combined with contact angle measurements, adsorption measurements, Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy characterizations. Single-mineral flotation results demonstrated that 3-MP reduced pyrite recovery to 19% while maintaining pentlandite recovery steadily at 75%. In artificial mixed-mineral flotation, 3-MP significantly upgraded the nickel concentrate grade, with a nickel recovery of 85.42%. Open-circuit flotation (one rougher, one scavenger and two cleaner stages) on a real ore yielded a nickel concentrate assaying 3.40% Ni and 1.73% Co, corresponding to enrichment ratios of 5.7-fold and 5.6-fold, respectively, and the sulfur recovery to the concentrate was merely 10.07%, indicating favorable practical application potential of this reagent. Surface analyses confirmed that 3-MP chemically bonds with Fe sites on the pyrite surface via its thiol group (–SH), while exhibiting negligible interaction with Ni sites on pentlandite, thereby leaving the surface properties and collector adsorption behavior of pentlandite unaffected and ensuring its excellent floatability. This work provides a theoretical basis and technical support for the efficient separation and utilization of nickel-cobalt sulfide resources. Download: Download high-res image (176KB) Download: Download full-size image

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PROCESS SAFETY AND ENVIRONMENTAL PROTECTION · 2026 · IF 7.9

Aerobic and anaerobic degradation of BDE-47 by facultative anaerobe Pseudomonas sp. QS-1: Pathway, product toxicity, and bio-augmentation remediation

Xin Qi,Ziwei Wang,Qixin Xia,Xiuping Liang,Guiyin Wang,Changlian Xu,Guochun Lv,Junzhuo Cai,Zhang Cheng,Zhanbiao Yang,Liling Wang,Xiaoxun Xu,Hua Yin

Although microbial degradation has been extensively studied for removing 2,2′,4,4′-tetrabrominated diphenyl ether (BDE-47), knowledge regarding the comparative efficiency and safety of degradation by facultative anaerobes under varying oxygen conditions remain limited. This study investigated the degradation of BDE-47 by Pseudomonas sp. strain QS-1 under both aerobic and anaerobic conditions. Our findings revealed that 47.5% and 12.4% of the initially added BDE-47 (0.5 mg/L) were transformed within 7 days under aerobic and anaerobic conditions, respectively. The aerobic transformation involved a complex pathway consisting of debromination, hydroxylation, ether bond cleavage, and ring opening, whereas the anaerobic transformation was limited to debromination. Toxicity assessments using an Escherichia coli model revealed that aerobic degradation products reduced cytotoxicity, whereas anaerobic degradation products induced higher rates of cell apoptosis than the parent BDE-47. Metabolomics analysis attributed this enhanced toxicity of anaerobic products to the specific inhibition of purine metabolism. In soil microcosm experiments, strain QS-1 exhibited stronger colonization and degradation performance under aerobic conditions, shifting the soil microbial community assembly towards more deterministic processes and strengthening network interactions with indigenous taxa. These findings provide insights into the biological effects of BDE-47 degradation products, and inform the assessment of efficacy and safety for bioremediation strategy. Download: Download high-res image (175KB) Download: Download full-size image

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Genes · 2026 ·Vol. 17 ·期 5 ·586 · IF 3.1

Identification of the PsEXP Gene Family and Functional Analysis of PsEXPA4-1 During Flower Opening Process in Tree Peony (Paeonia suffruticosa)

Jiayi Ying,Zhishuang Wang,Yinuo Shen,Yangdeng Lin,Yao Wang,Congying Zhu,Yiyang Xu,Luanfang Lin,Xiangtao Zhu,Xia Chen,Qianqian Wang

Background/Objectives: Tree peony (Paeonia suffruticosa) has a short flowering period, and its regulatory mechanisms remain poorly understood. These limitations have severely constrained its industrial development. Expansins (EXPs) are key proteins that mediate cell wall loosening associated with petal expansion, yet they remain uncharacterized in tree peony. Methods: This study utilized gene family identification, key gene screening and functional research, as well as regulatory network analysis to reveal the role of the EXP family in the regulation of flower opening. Results: This study presents the first genome-wide identification of 36PsEXPgenes in tree peony, classifying them into four evolutionarily conserved subfamilies (PsEXPA, PsEXPB, PsEXLA, and PsEXLB). Promoter analysis revealed that 28 out of 36PsEXPpromoters contain gibberellin (GA)-responsive elements. Exogenous GA3treatment significantly promoted flower opening and upregulated eightPsEXPs, withPsEXPA4-1showing the highest expression level and promoter GA-responsive element abundance. Subcellular localization confirmed that PsEXPA4-1 was targeted to the cell wall. Overexpression ofPsEXPA4-1inArabidopsisled to early flowering and enlarged petals, indicating thatPsEXPA4-1had the potential to promote cell expansion, consistent with its proposed role in tree peony flower opening. Mechanistically, we identified a bHLH transcription factor, PsbHLH25, whose expression was induced by GA. Y1H and dual-luciferase assays indicated that PsbHLH25 can bind to thePsEXPA4-1promoter. Conclusions: This study systematically characterized the EXP gene family in tree peony, revealedPsEXPA4-1as a key effector downstream of GA promoting flower opening, and discoveredPsbHLH25as a transcriptional activator linking GA signaling toPsEXPA4-1. These findings provided important insights into GA-mediated floral opening and genetic resources for understanding the molecular mechanisms and enabling precise flowering time regulation in tree peony.

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