INDUSTRIAL & ENGINEERING CHEMISTRY RESEARCH
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2019
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IF 3.375
Junjie Zhu,Linbo Wu,Zhiyang Bu,Suyun Jie,Bo-Geng Li
Searching for highly efficient and robust CO2 adsorbents is very important for CO2 capture, utilization, and storage. In this study, new polyethylenimine-grafted metal–organic framework (MOF)–polymer composites, abbreviated as PEI@PGD-H, were synthesized via high internal phase emulsion (HIPE) template polymerization of divinylbenzene and glycidyl methacrylate, followed by in situ generation of HKUST-type MOF in the presence of hydrophobic-modified CuO nanoparticles via the reaction of CuO with 1,3,5-benzenetricarboxylic acid and then polyethylenimine (PEI) functionalization via epoxy–amine reaction and amine–metal sites interaction. The coexistence of the hierarchical interconnected porous skeleton of poly(glycidyl methacrylate–divinylbenzene) (PGD), high specific surface area of MOF, and chemical CO2 adsorption of PEI endows PEI@PGD-H with high CO2 adsorption capacity, rate, and selectivity. PEI70@PGD-H shows a CO2/N2 separation factor as high as 76 and CO2 adsorption capacities of 4.3, 3.0, and 1.8 mmol of CO2/g from pure CO2, simulated flue gas, and air, respectively. After 20 CO2 adsorption–desorption cycles, the adsorbent still retained a high and stable CO2 capture capacity over 2.8 mmol of CO2/g for simulated flue gas. The adsorbent also displays reasonably good thermal stability, excellent water endurance, low desorption energy, and easy shaping. The desorption heat is as low as 48 kJ/mol of CO2. These features make PEI@PGD-H highly efficient, robust, and low-energy CO2 adsorbents for practical application in CO2 capture.
研究领域:
材料科学
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环境科学
✓ 已验证
产品关联
DOI
高影响因子
Medicine in Novel Technology and Devices
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2026
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IF 4.5
Yuqi Li,Jiawei Wang,Dongyan Li,Min Zhang,Lizhen Wang,Yubo Fan
Poly(glycerol dodecanoate) (PGD) is a biodegradable shape-memory elastomer that can be rendered magnetically responsive by incorporating Fe 3 O 4 . However, the effects of Fe 3 O 4 loading on degradation and biosafety remain unclear, which limits the in vivo translation of PGD/Fe 3 O 4 composites. This study aimed to clarify the relationship between Fe 3 O 4 content, degradation behavior, and gastrointestinal biosafety, thereby informing the design of PGD/Fe 3 O 4 devices. Five formulations containing 0, 5, 10, 20, or 40 wt% Fe 3 O 4 were prepared and designated as ION-0, ION-5, ION-10, ION-20, and ION-40. The composites were evaluated by FTIR, SEM/EDS, lipase-mediated degradation under dynamic and static conditions, Caco-2 assays, and 70-day oral exposure in mice. FTIR confirmed Fe 3 O 4 incorporation without altering the principal polyester backbone. Under both degradation conditions, the degradation percentage and medium acidification decreased with increasing Fe 3 O 4 content. Conditioned degradation media from ION-0, ION-5, ION-10, and ION-20 preserved Caco-2 viability and proliferation and maintained ZO-1 and Occludin expression, whereas ION-40 reduced junctional marker expression despite limited overt cytotoxicity. After daily gavage for 70 days, no obvious pathological lesions were observed in the heart, liver, spleen, lung, or kidney in any group, except for the intestine, where evident ileal injury and decreased ileal ZO-1 and Occludin expression were observed in the ION-40 group, whereas the other groups remained well tolerated. Overall, increasing Fe 3 O 4 loading improved structural persistence during degradation but narrowed the biosafety window. Within the present formulation set, composites containing up to 20 wt% Fe 3 O 4 provided the most favorable balance between degradation behavior and intestinal biosafety, supporting their further development for biomedical devices.
✓ 已验证
DOI
高影响因子
PHYTOMEDICINE
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2025
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IF 8.3
Yang Tang,Zheng Wang,Feng Zhou,Ling Li,Chen Sun,Linhui Li,Fei Tang,Dongqin Huang,Zewei Li,Yang Tan,Gang Pei
Background Ulcerative colitis (UC) is a clinically refractory diseases of the digestive system. Benzoylpaeoniflorin (BP) is a compound from Baishao, a Chinese herbal medicine documented with effects of anti-enteritis. However, the potential of BP in treating UC, along with its underlying mechanisms, requires further elucidation. Purpose This research was conducted to assess the effects of BP on dextran sulfate sodium (DSS)-induced UC and to elucidate its underlying mechanisms. Methods The C57BL/6 mouse model of UC was developed by administering the mice to freely drink DSS solution for 7 days. The mice were also subjected to intragastric administration of BP. Histopathology, nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, and ferroptosis indicators were determined in vivo . Besides, NCM460 cells were used to further evaluate the anti-ferroptosis effect of BP and its potential mechanisms. Ferroptosis agonists iron-dextrin (ID) and Erastin were employed to investigate whether BP exerts anti-UC effect by inhibiting ferroptosis. Similarly, Nrf2 inhibitor ML385 was conducted to ascertain the role of the Nrf2 signaling pathway in the downregulating ferroptosis effect of BP. Moreover, an ultra-performance liquid chromatography coupled with mass spectrometry was utilized to evaluate the changes in glucose metabolism within colon tissues of UC mice following BP treatment. Cellular thermal shift assay (CETSA), surface-plasmon resonance (SPR) and molecular docking were carried out to reveal the binding ability of BP and phosphogluconate dehydrogenase (PGD) protein. The PGD inhibitor, 6PGD-IN-S3 was used to evaluated whether BP inhibits anti-ferroptosis effect by upregulating the expression of PGD. Results BP exhibited significant anti-UC activity, leading to a reduction in both the disease activity index and histological damage in mice afflicted with UC. BP effectively mitigated DSS-induced ferroptosis both in vivo and in vitro . Additionally, ID and Erastin treatment diminished the therapeutic efficacy of BP against UC. A similar trend was observed in mice treated with ML385. Metabolomics analysis indicated that BP had a notable effect in restoring the pentose phosphate pathway (PPP) of colon tissues following DSS administration. The treatment of BP upregulated the activity of PGD. The inhibition of PGD weakened the anti-ferroptosis effect of BP. Subsequent analysis revealed that BP has the potential to effectively bind to PGD, thereby inhibiting PGD entries lysosomes. Conclusion The above findings provide robust evidence for the anti-UC mechanism of BP in inhibiting ferroptosis through upregulation of the Nrf2 signal. PGD, a key enzyme in the PPP, is proved as the target protein of BP to inhibit ferroptosis first time. BP has been further proved to inhibit the lysosomal degradation pathway of PGD.
研究领域:
药理学
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胃肠病学
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分子生物学
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生物化学
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中医学
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细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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