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JOURNAL OF MICROENCAPSULATION · 2020 · IF 2.287

Novel folated pluronic F127 modified liposomes for delivery of curcumin: preparation, release, and cytotoxicity

Ziling Li,Xiangyuan Xiong,Shengfeng Peng,Xing Chen,Wei Liu,Chengmei Liu

Aim: A novel folated pluronic F127 (FA-F127) was synthesised, so as to modify liposomes with FA group on the surface, and evaluate the effects of FA-F127 modification on the properties of the modified liposomes.Methods: FA was linked to one end of pluronic F127, via the terminal OH group, to obtain FA-F127 and the structure was characterised. FA-F127 modified curcumin liposomes (cur-FA-F127-Lps) were prepared. The physicochemical characteristics of cur-FA-F127-Lps, including morphology and particle size, were studied. The in vitro cytotoxicity of cur-FA-F127-Lps against KB cancer cells was determined by MTT tests.Results: The effects of FA-F127 modification on the average particle size, PDI, curcumin encapsulation efficiency and microstructure were not significant. Compared with nonfolated F127 liposomes (cur-F127-Lps), cur-FA-F127-Lps exhibited significantly higher cytotoxicity towards KB cells.Conclusions: Folic acid modified liposomes provide a novel strategy to improve the chemotherapeutic efficacy of hydrophobic bioactive compounds.

CAS / MDL: 458-37-7
研究领域: 药剂学 · 药物递送系统 · 纳米技术 · 肿瘤学
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ENVIRONMENT INTERNATIONAL · 2020 · IF 7.577

Evidence linking exposure of fish primary macrophages to antibiotics activates the NF-kB pathway

Wenhui Qiu,Jiaqi Hu,Jason T. Magnuson,Justin Greer,Ming Yang,Qiqing Chen,Meijuan Fang,Chunmiao Zheng,Daniel Schlenk

Low doses of antibiotics are ubiquitous in the marine environment and may exert negative effects on non-target aquatic organisms. Using primary macrophages of common carp, we investigated the mechanisms of action following exposure to several common antibiotics; cefotaxime, enrofloxacin, tetracycline, sulfamonomethoxine, and their mixtures, and explored the immunomodulatory effects associated with the nuclear factor-κB (NF-κB) signaling pathway. A KEGG pathway analysis was conducted using the sixty-six differentially expressed genes found in all treatments, and showed that exposure to 100 μg/L of antibiotics could affect regulation of the NF-κB signaling pathway, suggesting that activation of NF-κB is a common response in all four classes of antibiotics. In addition, the four antibiotics induced nf-κb and NF-κB-associated cytokines expression, as verified by qPCR, however, these induction responses by four antibiotics were minor when compared to the same concentration of LPS treatment (100 μg/L). Antagonists of NF-κB blocked many of the immune effects of the antibiotics, providing evidence that NF-κB pathways mediate the actions of all four antibiotics. Moreover, exposure to environmentally relevant, low levels (0.01–100 μg/L) of antibiotics induced a NF-κB-mediated immune response, including endogenous generation of ROS, activity of antioxidant enzymes, as well as expression of cytokine and apoptosis. Moreover, exposure to mixtures of antibiotics presented greater effects on most tested immunological parameters than exposure to a single antibiotic, suggesting additive effects from multiple antibiotics in the environment. This study demonstrates that exposure of fish primary macrophages to low doses of antibiotics activates the NF-kB pathway.

研究领域: 水生毒理学 · 免疫学 · 环境科学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Nanomaterials · 2016 ·Vol. 6 ·期 6 ·113 · IF 2.69

Targeting and Photodynamic Killing of Cancer Cell by Nitrogen-Doped Titanium Dioxide Coupled with Folic Acid

Jin Xie,Xiaobo Pan,Mengyan Wang,Longfang Yao,Xinyue Liang,Jiong Ma,Yiyan Fei,Pei-Nan Wang,Lan Mi

Titanium dioxide (TiO2) has attracted wide attention as a potential photosensitizer (PS) in photodynamic therapy (PDT). However, bare TiO2can only be excited by ultraviolet illumination, and it lacks specific targeting ligands, which largely impede its application. In our study, we produced nitrogen-doped TiO2and linked it with an effective cancer cell targeting agent, folic acid (FA), to obtain N-TiO2-FA nanoconjugates. Characterization of N-TiO2-FA included Zeta potential, absorption spectra and thermogravimetric analysis. The results showed that N-TiO2-FA was successfully produced and it possessed better dispersibility in aqueous solution than unmodified TiO2. The N-TiO2-FA was incubated with human nasopharyngeal carcinoma (KB) and human pulmonary adenocarcinoma (A549) cells. The KB cells that overexpress folate receptors (FR) on cell membranes were used as FR-positive cancer cells, while A549 cells were used as FR-negative cells. Laser scanning confocal microscopy results showed that KB cells had a higher uptake efficiency of N-TiO2-FA, which was about twice that of A549 cells. Finally, N-TiO2-FA is of no cytotoxicity, and has a better photokilling effect on KB cells under visible light irradiation. In conclusion, N-TiO2-FA can be as high-value as a PS in cancer targeting PDT.Keywords:titanium dioxide nanoparticle;photodynamic therapy;cancer cell targeting;folic acid

CAS / MDL: 919-30-2
研究领域: 纳米技术 · 癌症研究 · 材料科学 · 治疗学
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MOLECULES · 2019 ·Vol. 24 ·期 9 ·1661 · IF 3.06

Quantitative Structure–Activity Relationships for the Flavonoid-Mediated Inhibition of P-Glycoprotein in KB/MDR1 Cells

Mengmeng Xia,Yajing Fang,Weiwei Cao,Fuqiang Liang,Siyi Pan,Xiaoyun Xu

P-glycoprotein (P-gp) serves as a therapeutic target for the development of inhibitors to overcome multidrug resistance (MDR) in cancer cells. In order to enhance the uptake of chemotherapy drugs, larger amounts of P-gp inhibitors are required. Besides several chemically synthesized P-gp inhibitors, flavonoids as P-gp inhibitors are being investigated, with their advantages including abundance in our daily diet and a low toxicity. The cytotoxicity of daunorubicin (as a substrate of P-gp) to KB/MDR1 cells and the parental KB cells was measured in the presence or absence of flavonoids. A two-dimensional quantitative structure–activity relationship (2D-QSAR) model was built with a high cross-validation coefficient (Q2) value of 0.829. Descriptors including vsurf_DW23, E_sol, Dipole and vsurf_G were determined to be related to the inhibitory activity of flavonoids. The lack of 2,3-double bond, 3′-OH, 4′-OH and the increased number of methoxylated substitutions were shown to be beneficial for the inhibition of P-gp. These results are important for the screening of flavonoids for inhibitory activity on P-gp.Keywords:flavonoids;P-gp;inhibitory activity;QSAR

研究领域: 药理学 · 肿瘤学
✓ 已验证 DOI PubMed 高影响因子
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Polymers · 2021 ·Vol. 13 ·期 23 ·4210 · IF 4.329

Construction of KB@ZIF-8/PP Composite Separator for Lithium–Sulfur Batteries with Enhanced Electrochemical Performance

Bingyi Ma,Xin Zhang,Xiaoqian Deng,Sheng Huang,Min Xiao,Shuanjin Wang,Dongmei Han,Yuezhong Meng

Lithium–sulfur batteries (LSBs) have attracted wide attention, but the shuttle effect of polysulfide hinders their further practical application. Herein, we develop a new strategy to construct a Ketjen black@zeolite imidazole framework-8/polypropylene composite separator. Such a separator consists of Ketjen black (KB), zeolite imidazole framework-8 (ZIF-8) and polypropylene (PP) with a low coating load of 0.06 mg cm−2and is denoted as KB@ZIF-8/PP. KB@ZIF-8/PP can absorb polysulfides because of the Lewis acid-base interaction between ZIF-8 and polysulfides. This interaction can reduce the dissolution of polysulfides and suppress the shuttle effect, thereby enhancing the electrochemical performance of the battery. When tested at a current density of 0.1 C, an LSB with a KB@ZIF-8/PP separator exhibits low polarization and achieves a high initial capacity of 1235.6 mAh/g and a high capacity retention rate of 59.27% after 100 cycles.Keywords:lithium–sulfur battery;separator;shuttle effect;metal-organic framework;chemisorption

研究领域: 材料科学 · 电化学 · 能源存储
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Bioengineered · 2022 · IF 6.832

Identifying the shared genes and KEGG pathways of Resolvin D1-targeted network and osteoarthritis using bioinformatics

Wenjun Jiang,Xiaoying Wang,Siwei Su,Sen Du,Hongqiang Song

Osteoarthritis (OA) is a common chronic degenerative disease characterized by the loss of articular cartilage, which causes loss of joint function and reduce quality of life. Resolvin D1 (RvD1) has shown interesting anti-inflammatory effects; however, the mechanism of action of RvD1 in OA remains unclear. The aim of this study was to investigate the potential mechanism of RvD1 in OA by bioinformatics and partial in vitro mechanisms. Here, 106 shared differentially expressed genes (DEGs) were identified based on the GSE82107, GSE55235, GSE55457 dataset; 700 DEGs were identified based on GSE169077. Enrichment analyses of these genes were then successively conducted. RvD1-targeted genes and KEGG pathways are identified by STITCH. 27 shared KEGG pathways were identified among RvD1-targeted pathways and OA. Furthermore, cell apoptosis assay, western blotting, real-time fluorescent quantitative PCR (qRT-PCR), enzyme linked immunosorbent assay (ELISA) were used to confirm the expression levels of the key genes of shared Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways between RvD1-targeted and OA in IL-1β treated rat knee chondrocytes. The results showed that RvD1-targeted pathways and the expression of nuclear p65, p53, and p-JNK were inhibited in the RvD1 group compared with the IL-1β group. Thus, the findings indicate that RvD1 may inhibit the development of OA through NF/kB, p53, MAPK/JNK, PI3K-AKT signaling pathways, and act as a treatment for OA.

CAS / MDL: 5108-96-3
研究领域: 生物信息学 · 分子生物学 · 药理学 · 骨科
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JOURNAL OF MATERIALS SCIENCE · 2024 ·Vol. 59 ·期 21 ·9250-9264 · IF 3.5

Trace copper and bi-nonmetallic (N/S) modified ketjenblack (KB) as advanced electrocatalysts for oxygen reduction reactions

Liu Lvfei,Zhang Yao,Gu Yunjie,Qu Jiangwen,Wang Naiguang,Ge Shuaichen,Li Jingsha

The sluggish oxygen reduction reaction (ORR) has been one of the most majority bottlenecks of fuel cells and metal-air batteries. It is extremely desirable but challenging to explore low cost, highly active, stable catalysts toward ORR to replace commercial Pt/C catalysts. Herein, a novel hybrid system consisting of trace copper and bi-nonmetallic (N/S) modified the commercial ketjenblack (KB) carbon (Cu–NS–C) has been successfully fabricated by a pyrolysis of Cu–MOF/KB and thiourea to transform crystalline Cu/Cu 2 O nanoparticles into copper sulfide nanoparticles and the subsequent acid leaching. The optimized Cu–NS–C delivers a half-wave potential of 0.81 V versus RHE and a limiting-current density of 5.0 mA cm −2 , which is next to those of commercial 20 wt% Pt/C catalyst. Furthermore, this catalyst demonstrates much better durability and methanol tolerance than Pt/C catalyst.

CAS / MDL: 100-21-0 280-57-9
研究领域: 材料科学 · 能源化学
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ACS Applied Materials & Interfaces · 2023 · IF 9.5

Li2CO3 Nanocomposites as Cathode Lithium Replenishment Material for High-Energy-Density Li-Ion Batteries

Chenkun Li,Yao Xiao,Xiaosong Zhang,Hongwei Cheng,Ya-Jun Cheng,Yonggao Xia

The irreversible capacity loss of lithium-ion batteries during initial cycling directly leads to a decrease in energy density, and promising lithium cathode replenishment can significantly alleviate this problem. In response to the problems of complex preparation, instability in air, and unfavorable residue of the conventional cathode lithium replenishment materials, a Li2CO3/carbon nanocomposite is prepared and utilized as the lithium replenishment material. With high-speed ball-milling, a nanocomposite with a tight embedment structured Li2CO3/Ketjen Black (KB) composite composed of nanosized Li2CO3 and KB is synthesized. The decomposition potential of Li2CO3 is effectively decreased to 3.8 V, and the amount of the active lithium ion being released is significantly increased, corresponding to a specific capacity of 645.2 mAh·g–1 during the initial charging cycle. It has been introduced into the full-cells composed of the NCM523 cathode and graphite anode, resulting in a capacity increase of 44 mAh·g–1 in the initial cycle and a 26.4% improvement in capacity retention over 100 cycles. The working mechanism of the Li2CO3/KB nanocomposite as the lithium replenishment agent has been discussed. The outcome of the work provides a practically feasible route to realize lithium-ion battery technology with improved energy density and cycling life.

CAS / MDL: 872-50-4
研究领域: 材料科学 · 能源技术
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CANCER LETTERS · 2023 · IF 9.7

A multi-functional nano-system combining PI3K-110α/β inhibitor overcomes P-glycoprotein mediated MDR and improves anti-cancer efficiency

Ruikun Lin,Lei Zhang,Biwei Ye,Yanan Wang,Yi-Dong Li,Hsu Jason,Wenzhen Liu,Ping Hu,Jincan Chen,Zhe-Sheng Chen,Zhuo Chen

P-glycoprotein (P-gp/ABCB1)-mediated multidrug resistance (MDR) in cancers severely limit chemotherapeutic efficacy. We recently reported that phosphatidylinositol-3-kinase (PI3K) 110α and 110β subunits can be novel targets for reversal of P-gp mediated MDR in cancers, and BAY-1082439 as an inhibitor specific for PI3K 110α and 110β subunits could reverse P-gp-mediated MDR by downregulating P-gp expression in cancer cells. However, BAY-1082439 has very low solubility, short half-life and high in-vivo clearance rate. Till now, nano-system with the functions to target PI3K P110α and P110β and reverse P-gp mediated MDR in cancers has not been reported. In our study, a tumor targeting drug delivery nano-system PBDF was established, which comprised doxorubicin (DOX) and BAY-1082439 respectively encapsulated by biodegradable PLGA-SH nanoparticles (NPs) that were grafted to gold nanorods (Au NRs) modified with FA-PEG-SH, to enhance the efficacy to reverse P-gp mediated MDR and to target tumor cells, further, to enhance the efficiency to inhibit MDR tumors overexpressing P-gp. In-vitro experiments indicated that PBDF NPs greatly enhanced uptake of DOX, improved the activity to reverse MDR, inhibited the cell proliferation, and induced S-phase arrest and apoptosis in KB-C2 cells, as compared with free DOX combining free BAY-1082439. In-vivo experiments further demonstrated that PBDF NPs improved the anti-tumor ability of DOX and inhibited development of KB-C2 tumors. Notably, the metastasis of KB-C2 cells in livers and lungs of nude mice were inhibited by treatment with PBDF NPs, which showed no obvious in-vitro or in-vivo toxicity.

CAS / MDL: 9002-89-5
研究领域: 肿瘤学 · 药理学 · 纳米技术 · 癌症研究
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES · 2024 · IF 7.7

Therapeutic potential of proteases in acute lung injury and respiratory distress syndrome via TLR4/Nrf2/NF-kB signaling modulation

Hend Mohamed Anwar,Gad Elsayed Mohamed Salem,Hanan M. Abd El-Latief,Amany Abd Elhameid Osman,Sahar K. Ghanem,Haroon Khan,Suchana Chavanich,Alshaymaa Darwish

The COVID-19 pandemic has drawn attention to acute lung injury and respiratory distress syndrome as major causes of death, underscoring the urgent need for effective treatments. Protease enzymes possess a wide range of beneficial effects, including antioxidant, anti-inflammatory, antifibrotic, and fibrinolytic effects. This study aimed to evaluate the potential therapeutic effects of bacterial protease and chymotrypsin in rats in mitigating acute lung injury induced by lipopolysaccharide . Molecular docking was employed to investigate the inhibitory effect of bacterial protease and chymotrypsin on TLR-4, the receptor for lipopolysaccharide. Bacterial protease restored TLR-4, Nrf2 , p38 MAPK , NF-kB, and IKK-β levels to normal levels, while chymotrypsin normalized TLR-4, IKK-β, IL-6, and IL-17 levels. The expression of TGF-β, caspase-3, and VEGF in the bacterial protease- and chymotrypsin-treated groups was markedly reduced. Our results suggest that both therapies ameliorate LPS-induced acute lung injury and modulate the TLR4/Nrf2/NF-k signaling pathway. Each protease exhibited distinct mechanisms, with bacterial protease showing a better response to oxidative stress, edema, and fibrosis , whereas chymotrypsin provided a better response in the acute phase and innate immunity. These findings highlight the potential of each protease as a promising therapeutic option for acute lung injury and respiratory distress syndrome.

研究领域: 医学 · 药理学 · 分子生物学
✓ 已验证 DOI PubMed 高影响因子
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INTERNATIONAL IMMUNOPHARMACOLOGY · 2025 · IF 4.7

Perillaldehyde protect chondrocytes from mitophagy-associated apoptosis and NLRP3-mediated inflammation by regulating ALOX5/NF-kB signaling in osteoarthritis

Qingqi Zhou,Xun Li,Decai Hou

Background Osteoarthritis (OA) is an age-related progressive joint disease characterized by loss of cartilage and subsequent inflammation. Perillaldehyde is a compound extracted from Perilla , which has multiple pharmacological activities including anti-inflammatory, and anti-apoptosis. However, it still remains unknown whether and how perillaldehyde could regulate chondrocyte apoptosis and inflammation in OA. Methods The interleukin-1beta (IL-1β)-treated chondrocytes and destabilized medial meniscus (DMM) -induced rats were used as in vitro and in vivo models of OA. Cell viability, proliferation, and apoptosis were investigated by cell counting kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU) and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays. The mitochondrial membrane potential was analyzed by 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining. Light chain 3 (LC3) location, and expression of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) were detected by immunofluorescence staining. Relative protein levels were measured via western blotting. Tumor necrosis factor-alpha (TNF-α), IL-6 and IL-8 levels were measured by enzyme-linked immunosorbent assay (ELISA). The cartilage injury in rats was investigated via hematoxylin-eosin (HE) staining. Results Perillaldehyde attenuated IL-1β-induced inhibition of viability (from 44.45 % to 92.72 %, p  < 0.05) and proliferative potential of chondrocytes ( p  < 0.05). Perillaldehyde mitigated mitophagy-associated apoptosis of chondrocytes by enhancing mitophagy ( p  < 0.05) and reducing cell apoptosis (from 32.36 % to 8.00 %, p  < 0.05). Perillaldehyde attenuated NLRP3-mediated inflammation through reducing NLRP3, ASC, TNF-α, IL-6 and IL-8 levels ( p  < 0.05). ALOX5 expression was upregulated in OA (fold change: 2.61, p  < 0.05), and decreased by perillaldehyde treatment (fold change: 1.34, p  < 0.05). Perillaldehyde inhibits p65 nuclear factor kappa B (NF-κB) signaling activation (fold change: 3.19 to 1.33, p  < 0.05) by regulating ALOX5 expression. ALOX5 overexpression reversed the effects of perillaldehyde on mitophagy-associated apoptosis and NLRP3-mediated inflammation ( p  < 0.05), and these roles were mitigated due to NF-κB inactivation ( p  < 0.05). Perillaldehyde attenuated cartilage injury in OA rats ( p  < 0.05). Conclusion Perillaldehyde attenuated IL-1β-induced mitophagy-associated apoptosis and NLRP3-mediated inflammation through decreasing ALOX5 and inactivating NF-κB signaling, indicating the potentially protective potential of perillaldehyde in osteoarthritis.

CAS / MDL: 30525-89-4
研究领域: 医学 · 药理学
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JOURNAL OF PHARMACOLOGICAL SCIENCES · 2025 · IF 2.9

Sulfasalazine disrupts the interaction between TNFα and TNFR1 thus inhibiting NF-kB signaling activation to promote bone fracture healing

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.

CAS / MDL: 599-79-1
研究领域: 药理学 · 分子生物学 · 免疫学 · 骨科学 · 细胞生物学
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