Nano Research
·
2024
·Vol. 17
·期 7
·5786-5794
·
IF 9.5
Yang Chaoxin,Cai Zhengwei,Liang Jie,Dong Kai,Li Zixiao,Sun Hang,Sun Shengjun,Zheng Dongdong,Zhang Hui,Luo Yongsong,Yao Yongchao,Wang Yan,Ren Yuchun,Liu Qian,Li Luming,Chu Wei,Sun Xuping,Tang Bo
Seawater electrolysis, especially in coastlines, is widely considered as a sustainable way of making clean and high-purity H 2 from renewable energy; however, the practical viability is challenged severely by the limited anode durability resulting from side reactions of chlorine species. Herein, we report an effective Cl − blocking barrier of NiFe-layer double hydroxide (NiFe-LDH) to harmful chlorine chemistry during alkaline seawater oxidation (ASO), a pre-formed surface-derived NiFe-phosphate (Pi) outer-layer. Specifically, the PO 4 3− -enriched outer-layer is capable of physically and electrostatically inhibiting Cl − adsorption, which protects active Ni 3+ sites during ASO. The NiFe-LDH with the NiFe-Pi outer-layer (NiFe-LDH@NiFe-Pi) exhibits higher current densities ( j ) and lower overpotentials to afford 1 A·cm −2 ( η 1000 of 370 mV versus η 1000 of 420 mV) than the NiFe-LDH in 1 M KOH + seawater. Notably, the NiFe-LDH@NiFe-Pi also demonstrates longer-term electrochemical durability than NiFe-LDH, attaining 100-h duration at the j of 1 A·cm −2 . Additionally, the importance of surface-derived PO 4 3− -enriched outer-layer in protecting the active centers, γ-NiOOH, is explained by ex situ characterizations and in situ electrochemical spectroscopic studies.
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JOURNAL OF MEDICINAL CHEMISTRY
·
2025
·
IF 6.8
Hang Zhang,Yujie Zhang,Yinping Geng,Xuanlong Zhen,Xiaodi Wang,Qiange Yin,Peng Zhang,Yuanyuan Li,Mengzhen Zhang,Yi-chao Zheng,Bing-rui Liu,Hui-min Liu,Hai-wei Xu
Gastric cancer is one of the major health threats to human beings and has a low response rate to emerging immunotherapy. We herein reported a novel indole-based LSD1-targeted antigastric agent 7ae, which was able to enhance the sensitivity of gastric cancer cells to a T-cell-mediated immune response. It exhibited potent LSD1 inhibitory activity (IC50 = 0.080 ± 0.002 μM) and reduced the expression of PD-L1, which in turn promoted the T-cell killing response in gastric cancer cells. As a result, 7ae acted as an active LSD1 inhibitor, exerting excellent anti-invasion and anti-migration effects in gastric cancer cells and leading to significant suppression of the growth of xenograft gastric tumors without obvious toxicity in vivo. Collectively, 7ae has been demonstrated to be a novel, potent LSD1 inhibitor with the potential to be used as an antigastric agent, as well as a useful tool compound for exploratory studies of T-cell-mediated immunity and/or immunotherapy in gastric cancer.
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CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Lv Xi,Xu Xincheng,Peng Yang,Li Bolin,Yang Lie,He Xiaoman
This study introduces a novel modification method for micron-sized zero-valent iron, utilizing Shewanella oneidensis MR-1 to simultaneously colonize its surface, disrupt the passivation layer, and alter the crystal structure of the core. This process yields a composite that retains its reducing activity even in high concentrations of pollutants (500 ppm Cr(VI)) and under neutral to slightly acidic conditions. Our findings indicate that the modified system induces the Kirkendall effect in zero-valent iron, leading to the formation of amorphous zero-valent iron with a non-spherical core structure, in contrast to conventional direct mixing approaches. The modified system achieves complete reduction of 100 ppm Cr(VI) to Cr(III) within 8 h. Notably, within the first 4 h of reaction, the reduction rate is approximately three times higher than that of the conventional direct mixing system. XPS, XRD, SEM, EEM and TEM analyses reveal that the surface passivation layer of the biochemically modified zero-valent iron is disrupted, leading to changes in its crystal structure, the formation of hollow spherical structures, and the development of a biological protective film on its surface. Interestingly, electrochemical and ETSA analyses indicate that the electron transfer rate of the biochemically modified composite is significantly enhanced. This study provides fundamental insights into the removal of Cr(VI) from groundwater using biochemically modified micron-sized zero-valent iron (mZVI).
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ACS Applied Materials & Interfaces
·
2025
·
IF 8.2
Juntao Huang,Saifei Wang,Zhifei Zhang,Mingli Chen,Han Wang,Haihua Huang,Qian Wang,Jigong Hao,Wei Li,Juan Du,Mahesh Kumar Joshi,Peng Fu
Ceramic dielectric capacitors have gained significant attention due to their ultrahigh power density, current density, and ultrafast charge–discharge speed. However, their potential applications have been limited by their relatively low energy storage density. Researchers have employed various approaches to enhance their energy storage density. In this study, (1 – x)(Bi0.5Na0.5)0.7Sr0.3TiO3–xCa(Mg1/3Ta2/3)O3 ceramics were prepared via a solid-phase reaction, and the effect of their structure on the energy storage properties was investigated. The results indicate that the introduction of Ca(Mg1/3Ta2/3)O3 significantly alters the multiscale structures of the (Bi0.5Na0.5)0.7Sr0.3TiO3 ceramic, including the transformation from the T-phase to the C-phase, refinement of ceramic grains, and the formation of polar nanoregions (PNRs), accompanied by an increase in the bandgap and relaxation degree. These structural changes collectively contributed to the improved overall energy storage properties of the modified ceramics. Notably, the 0.92(Bi0.5Na0.5)0.7Sr0.3TiO3–0.08Ca(Mg1/3Ta2/3)O3 ceramic demonstrated a recoverable energy storage density (Wrec) of 8.37 J/cm3 with an energy storage efficiency (η) of 87.7% at an electric field of 530 kV/cm. It also exhibited good temperature stability (25–120 °C), frequency stability (1–100 Hz), and fatigue stability (1–105). Furthermore, it displayed exceptional charge and discharge properties, with the discharge energy density (WD), discharge time (t0.9), current density (CD), and power density (PD) attaining 4.06 J/cm3, 35.2 ns, 2143.28 A/cm2, and 460.71 MW/cm3, respectively. These findings suggest that modified (1 – x)(Bi0.5Na0.5)0.7Sr0.3TiO3–xCa(Mg1/3Ta2/3)O3 ceramics are promising candidates for high-power pulsed electronic systems.
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JOURNAL OF MOLECULAR STRUCTURE
·
2025
·
IF 4.7
Zengfeng Wei,Yumeng Zhang,Hu Xia,Lijie Ni,Wenhai Wu,Xiaoning Wang,Heng Quan
A novel bio-based corrosion inhibitor, hexadecyl amine-modified catechol (CA16), was synthesized, and its molecular structure was characterized. The ability of CA16 to inhibit the corrosion of carbon steel in 1 M HCl was evaluated by potentiodynamic polarization, electrochemical impedance spectroscopy and weight loss. The highest inhibition efficiency reached 96.87% at 10 −3 M. CA16 is a mixed-type corrosion inhibitor that can adsorb on the Fe surface spontaneously through chemical adsorption following the Langmuir adsorption model. The adsorption of CA16 and carbon steel occurred between catechol groups and the Fe surface, as confirmed by quantum chemical calculations and molecular dynamic simulations. This novel bio-derived high-performance inhibitor offers a sustainable alternative to conventional petrochemical-based counterparts, demonstrating significant potential for industrial-scale applications while aligning with green chemistry principles.
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Pharmaceuticals
·
2025
·Vol. 18
·期 4
·548
·
IF 4.8
Huiming Xue,Zhen Feng,Chang Jin,Yue Zhang,Yongxing Ai,Jing Wang,Meizhu Zheng,Dongfang Shi
Objectives: Ischemic stroke is a severe neurological disorder with high morbidity, mortality, and disability rates, posing a substantial burden on patients, families, and healthcare systems. Soy isoflavone (SI), a naturally occurring phytoestrogen, has demonstrated promising neuroprotective effects. This study aimed to evaluate the anti-stroke efficacy of SI and elucidate its underlying mechanisms through integrated phytochemical profiling, network pharmacology, and both in vitro and in vivo experimental validation.Methods: Active constituents of SI were extracted via reflux and identified using liquid chromatography–mass spectrometry (LC-MS). Network pharmacology was employed to predict therapeutic targets and signaling pathways. The neuroprotective effects of SI were first assessed in PC12 cells subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) injury in vitro. For in vivo evaluation, transient cerebral ischemia–reperfusion injury was induced using the bilateral common carotid artery occlusion (BCCAO) model in adult male ICR rats (27.3 ± 1.8 g; 6–8 weeks old), obtained from the Shanghai Experimental Animal Center, Chinese Academy of Sciences. Forty-eight rats were randomly assigned into four groups (n= 12): sham, model (BCCAO), SI-treated (100 mg/kg, oral gavage for 5 days), and edaravone (EDA)-treated (10 mg/kg, i.p., positive control). All procedures were approved by the Institutional Animal Care and Use Committee of Changchun Normal University (Approval No. 2024003, 13 March 2024) and conducted in accordance with the NIH guidelines and ARRIVE 2.0 reporting standards.Results: In vitro, SI significantly enhanced PC12 cell viability from 57.23 ± 2.88% to 80.76 ± 4.43% following OGD/R. It also reduced intracellular Ca2+by 58.42%, lactate dehydrogenase (LDH) release by 37.67%, caspase-3 activity by 55.05%, and reactive oxygen species (ROS) levels by 74.13% (p< 0.05). A flow cytometry analysis revealed that OGD/R increased the apoptosis rate from 5.34% (control) to 30.85% (model group), which was significantly attenuated by SI treatment, especially in the 560 µg/mL group (20.00%), followed by the 140 and 280 µg/mL groups. In vivo, SI improved neurological scores from 8.3 ± 1.09 to 6.8 ± 1.68, reduced cerebral infarction volume by 18.49%, and alleviated brain edema by 10.42% (p< 0.05). SI also decreased malondialdehyde (MDA) and LDH levels by 31.15% and 39.46%, respectively, while increasing the activity of antioxidant enzymes: superoxide dismutase (SOD) by 11.70%, catalase (CAT) by 26.09%, and glutathione peroxidase (GSH-px) by 27.55% (p< 0.01). Scratch assay results showed that SI restored the impaired migratory ability of the OGD/R-treated PC12 cells, further supporting its role in cellular repair. A Western blot analysis demonstrated the upregulation of nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1) and the downregulation of Kelch-like, ECH-associated protein 1 (Keap1) in the cerebral ischemia–reperfusion model.Conclusions: These findings indicate that soy isoflavone confers significant neuroprotective effects against cerebral ischemia–reperfusion injury by enhancing endogenous antioxidant defense mechanisms, reducing oxidative stress, inhibiting apoptosis, and promoting cell migration. The protective effects are likely mediated through the activation of the Nrf2/Keap1 signaling pathway, supporting the therapeutic potential of SI in ischemic stroke treatment.
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FOOD CHEMISTRY
·
2024
·
IF 8.5
Siqi Peng,Jing Wang,Mohamed A. Farag,Mahmoud Salah,Lianliang Liu,Yajing Fang,Weimin Zhang
This study investigated the changes in phytochemical composition and inflammatory response of crude papaya ( Carica papaya L.) seed oil (CPO) and its refined forms (degummed, PDG; deacidified, PDA; decolorized, PDC; deodorized, PDO). Oils were analyzed for their phytochemical composition, oil quality parameters, antioxidant activity , and their inflammatory response in LPS-stimulated THP-1 macrophages. At higher refining degrees, particularly after deacidification , the contents of phytochemicals (sterols, tocopherols , and polyphenols) decreased while oxidation products increased. Both CPO (0.1–1.0 mg/mL) and PDG reduced the secretion and mRNA expression of LPS-stimulated inflammatory cytokines and mediators and also blocked the activation of the NF-κB pathway. PDA, PDC, and PDO showed low anti-inflammatory or even pro-inflammatory activity. Correlation analysis showed that 4 polyphenols and 2 phytosterols were responsible for the oil's anti-inflammatory effects. These findings indicated that moderate refining is suggested for papaya seed oil processing for retaining bioactive ingredients and anti-inflammatory ability.
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Food & Function
·
2025
·
IF 5.4
Qi Gu,Litao Wang,Mingyue Xu,Wan-Mei Zhou,Guosheng Liu,Haiting Tian,Thomas Efferth,Chenlu Wang,Yujie Fu
Phloretin is a natural dihydrochalcone with a variety of biological activities. Its potential in modulating lipid metabolism in vitro and in vivo with HepG2 and C. elegans was investigated in this study. Phloretin significantly diminished lipid accumulation and ROS levels, mitigated the degree of lipid peroxidation, and ameliorated mitochondrial dysfunction in HepG2 cells. The expression levels of lipid synthesis genes (SREBP and FASN) were downregulated, while PI3K-AKT related genes (AKT, FOXO, MTOR) were upregulated. Furthermore, phloretin significantly alleviated the detrimental effects of lipid accumulation on growth indices and locomotor ability in C. elegans. It also reduced lipofuscin, ROS level as well as glucose and triglyceride contents, significantly affected amino acid and lipid metabolism pathways based on metabolomics profiles and analysis. Gene expression levels of sbp-1, mdt-15, fat-5, fat-6, and fat-7 were markedly down-regulated following treatment with phloretin, while daf-16, age-1 and skn-1were significantly up-regulated. Tests with mutant C. elegans strains of daf-16, age-1, sbp-1 and nhr-49 further confirmed that the phloretin-induced decrease in lipid accumulation was attributed to the inhibition of lipid biosynthesis pathway by IIS and sbp-1/SREBP. Our study indicated that phloretin exerted hypolipidemic effects in vitro and in vivo, providing a basic foundation for considering phloretin as a phytochemical candidate for regulating lipid metabolism and preventing hyperlipidemia.
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Frontiers in Pharmacology
·
2025
·
IF 4.8
Gang Zhao,Yajuan Li,Mengyuan Liu,Wei Chang,Hui Shen,Junhui Xue,Fengzhou Liu
Objective: This study investigates the effects of acute hypobaric hypoxia (HH) on the anti-fatigue properties of pitolisant and explores the underlying mechanisms. The aim is to provide a theoretical basis for expanding its clinical indications and optimizing its use in individuals exposed to HH conditions.Methods: The anti-fatigue effects of pitolisant were evaluated using the water maze, novel object recognition, and rotating rod tests. Drug concentrations and dopamine levels were analyzed using High-Performance Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (HPLC-MS/MS). Additionally, gene and protein expression levels of P-glycoprotein (P-gp) and organic cation transporter 1 (OCT1) were assessed to explore the mechanisms by which HH affects pitolisant’s pharmacodynamics.Results: A 40 mg/kg dose of pitolisant significantly improved learning, memory, cognitive, and motor functions in sleep-deprived mice under HH conditions (P < 0.05). Pharmacokinetic analysis revealed a reduction in pitolisant concentration in the brain under HH conditions. Furthermore, OCT1 protein expression decreased after 1 h and 1 day of HH exposure (P < 0.05), while P-gp expression decreased after 1 h (P < 0.05).Conclusion: HH possibly reduced pitolisant’s brain concentration and efficacy by altering the expression of OCT1 and P-gp transporters. A 40 mg/kg dose was necessary for an effective anti-fatigue response. Pitolisant shows potential for supporting circadian rhythm regulation in shift workers and individuals suffering from jet lag. When used under HH conditions, adjusting the dose and frequency may be necessary due to altered pharmacokinetics.
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INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2018
·Vol. 43
·期 1
·103-116
·
IF 2.784
Zhi‑Jun Jiang,Qing‑Hua Shen,Hai‑Yong Chen,Zhe Yang,Ming‑Qi Shuai,Shu‑Sen Zheng
Liver fibrosis is a serious threat to human health, and there is currently no effective clinical drug for treatment of the disease. Although Galectin‑1 is effective, its role in liver function, inflammation, matrix metalloproteinases and the activation of hepatic stellate cells (HSCs) remains to be elucidated. The aim of the present study was to elucidate the effect of Galectin‑1 on the activation, proliferation and apoptosis of HSCs in a mouse model of liver fibrosis. Following successful model establishment and tissue collection, mouse HSCs (mHSCs) were identified and an mHSC line was constructed. Subsequently, to determine the role of Galectin‑1 in liver fibrosis, the expression levels of transforming growth factor (TGF)‑β1, connective tissue growth factor (CTGF) and α‑smooth muscle actin (α‑SMA) pre‑ and post‑transfection were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blot analyses. In addition, the effects of Galectin‑1 on the biological behavior and mitochondrial function of mHSCs were determined using a 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay, flow cytometry and a scratch test. It was first observed that the expression levels of Galectin‑1, TGF‑β1, CTGF and α‑SMA were downregulated by silencing the gene expression of Galectin‑1. Additionally, silencing the gene expression of Galectin‑1 inhibited cell cycle progression, proliferation and migration but induced the apoptosis of mHSCs from mice with liver fibrosis. Furthermore, the in vivo experimental results suggested that silencing the gene expression of Galectin‑1 improved liver fibrosis. Collectively, it was concluded that silencing the gene expression of Galectin‑1 ameliorates liver fibrosis and that functionally suppressing Galectin‑1 may be a future therapeutic strategy for liver fibrosis.
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BIOLOGICAL PROCEDURES ONLINE
·
2022
·Vol. 24
·期 1
·1-16
·
IF 7.717
Mei Jie,Cai Yun,Xu Rui,Yu Xinqian,Han Xu,Weng Miaomiao,Chen Lingyan,Ma Tao,Gao Tianshu,Gao Fei,Xia Tiansong,Zhu Yichao,Zhang Yan
Background Angiotensin-converting enzyme 2 (ACE2) is known as a tumor suppressor and lowly expressed in most cancers. The expression pattern and role of ACE2 in breast cancer (BC) have not been deeply elucidated. Methods A systematic pan-cancer analysis was conducted to assess the expression pattern and immunological role of ACE2 based on RNA-sequencing (RNA-seq) data downloaded from The Cancer Genome Atlas (TCGA). The correlation of ACE2 expression and immunological characteristics in the BC tumor microenvironment (TME) was evaluated. The role of ACE2 in predicting the response to therapeutic options was estimated. Moreover, the pharmacodynamic effect of angiotensin-(1–7) (Ang-1–7), the product of ACE2, on chemotherapy and immunotherapy was evaluated on the BALB/c mouse BC model. In addition, the plasma samples from BC patients receiving neoadjuvant chemotherapy were collected and subjected to the correlation analysis of the expression level of Ang-1–7 and the response to neoadjuvant chemotherapy. Results ACE2 was lowly expressed in BC tissues compared with that in adjacent tissues. Interestingly, ACE2 was shown the highest correlation with immunomodulators, tumor-infiltrating immune cells (TIICs), cancer immunity cycles, immune checkpoints, and tumor mutation burden (TMB) in BC. In addition, a high level of ACE2 indicated a low response to endocrine therapy and a high response to chemotherapy, anti-ERBB therapy, antiangiogenic therapy and immunotherapy. In the mouse model, Ang-1–7 sensitized mouse BC to the chemotherapy and anti-PD-1 immunotherapy, which revealed its significant anti-tumor effect. Moreover, a high plasma level of Ang-1–7 was associated with a better response to neoadjuvant chemotherapy. Conclusions ACE2 identifies immuno-hot tumors in BC, and its enzymatic product Ang-1–7 sensitizes BC to the chemotherapy and immunotherapy by remodeling the TME.
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Bioengineered
·
2021
·
IF 3.269
Yan Li,Nianling Yao,Yan Gao,Yunping Wang,Lu Bai,Jia Xu,Haixu Wang
Polycystic ovary syndrome (PCOS) is a common endocrine disorder that poses a great threat to women's health. MiR-1224-5p is downregulated in the follicular fluid of patients with PCOS, but its role remains largely unknown. In this study, mice were treated with dehydroepiandrosterone (DHEA) to establish an in vivo model of PCOS. We found that enhanced activation of NLRP3 inflammasome was accompanied by downregulation of miR-1224-5p in ovarian tissue of PCOS mice. The effect of miR-1224-5p was further explored in TNF-α-treated human granulosa-like tumor (KGN) cells. Upregulation of miR-1224-5p suppressed TNF-α-induced secretion of DHEA and testosterone. MiR-1224-5p attenuated TNF-α-induced inflammation by inhibiting NLRP3 inflammasome activation, IL-1β synthesis, and nuclear factor kappa B (NF-κB) p65 nuclear translocation. Notably, miR-1224-5p decreased the expression of Forkhead box O 1 (FOXO1) and its downstream gene thioredoxin interaction protein (TXNIP). Luciferase reporter assay confirmed FOXO1 as a target of miR-1224-5p. Upregulation of FOXO1 abolished miR-1224-5p-induced activation of NLRP3 inflammasome, demonstrating that miR-1224-5p might inhibit NLRP3 inflammasome activation through regulating FOXO1. This study provided novel insights into the pathogenesis of PCOS and suggested that miR-1224-5p might be a promising target for treating PCOS.
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