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A series of rhodamine B (RhB) encapsulated zeolitic imidazolate framework-8 (RhB@ZIF-8) composite nanomaterials with different concentrations of guest loadings have been synthesized and characterized in order to investigate their applicability to solid-state white-light-emitting diodes (WLEDs). The nanoconfinement of the rhodamine B dye (guest) in the sodalite cages of ZIF-8 (host) is supported by fluorescence spectroscopic and photodynamic lifetime data. The quantum yield (QY) of the luminescent RhB@ZIF-8 material approaches unity when the guest loading is controlled at a low level: 1 RhB guest per ~7250 cages. We show that the hybrid (luminescent guest) LG@MOF material, obtained by mechanically mixing a suitably high-QY RhB@ZIF-8 red emitter with a green-emitting fluorescein@ZIF-8 "phosphor" with a comparably high QY, could yield a stable, intensity tunable, near-white light emission under specific test conditions described. Our results demonstrate a novel LG@MOF composite system exhibiting a good combination of photophysical properties and photostability, for potential applications in WLEDs, photoswitches, bioimaging and fluorescent sensors. [ABSTRACT FROM AUTHOR]

Background: Psoriasis is a chronic, immune-mediated inflammatory skin disease, and the inflammatory response plays an important role in its development and progression. Datura metel L. is a traditional Chinese medicine that exhibited a significant therapeutic effect on psoriasis in our previous study due to its remarkable anti-inflammatory effect. Meanwhile, the mechanism underlying its effects on psoriasis is still unclear. Methods: An imiquimod-induced psoriasis-like dermatitis mouse model was constructed to evaluate the protective effect of the effective part of Datura metel L. (EPD), which was verified by evaluations of the Psoriasis Area and Severity Index (PASI) score. Hematoxylin and eosin (H&E) staining, immunohistochemical examination, enzyme-linked immunosorbent assay (ELISA), and Western blot were used to measure the inflammatory cytokines and the protein expression associated with the Toll-like receptor 7– myeloid differentiation primary response gene 88–nuclear Factor-κB–nucleotide-binding oligomerization domain (Nod)-like receptor family pyrin domain-containing 3 (TLR7/8–MyD88–NF-κB–NLRP3) inflammasome pathway. Results: EPD significantly decreased the PASI, reduced epidermal thickness, and decreased the proliferation and differentiation of epidermal cells in psoriasis-like dermatitis C57BL/6 mice induced by imiquimod (IMQ). Furthermore, EPD reduced the infiltration of CD3+ cells to psoriatic lesions, as well as ameliorated the elevations of intercellular adhesion molecule 1 (ICAM-1) and inhibited the production of imiquimod-induced inflammatory cytokines, including IL-1β, IL-2, IL-6, IL-10, IL-12, IL-17, IL-22, IL-23, tumor necrosis factor-α (TNF-α), monocyte chemotactic protein 1 (MCP-1), and interferon-γ (IFN-γ). Besides, EPD decreased the imiquimod-induced expression levels of TLR7, TLR8, TRAF6, MyD88, p-IKKα, p-IKBα, p-NF-κB, NLRP3, apoptosis-associated speck-like protein contained a caspase recruitment domain (ASC), cysteinyl aspartate specific proteinase 1 (caspase-1), and IL-1β. Conclusion: This study demonstrated that EPD exhibited a protective effect on an imiquimod-induced psoriasis mice model by inhibiting the inflammatory response, which might be ascribed to the inhibition of the TLR7/8–MyD88–NF-κb–NLRP3 inflammasome pathway. [ABSTRACT FROM AUTHOR]