Organic
solid materials with color-tunable emissions have been
extensively applied in various fields. However, a rational design
and facile synthesis of an ideal fluorophore are still challenging
due to the undesirable aggregation-caused quenching effect in concentrated
solution and solid form. Herein, we have developed a series of 2-(2′-hydroxyphenyl)benzothiazole
(HBT)-derived color-tunable solid emitters by switching
functional groups at the ortho-position of a hydroxyl group via formylation
and an aldol condensation reaction. By tuning the electron-withdrawing
ability and the π-conjugated framework introduced by the functional
groups, fluorophores emit light covering the full-color range from
blue to near-infrared regions with high quantum yields in their solid
form and show a significant solvatochromic effect in polar solvents.
The aggregation-induced emission (AIE) or aggregation-induced emission
enhancement (AIEE) and excited-state intramolecular proton transfer
(ESIPT) involving fluorescence mechanism, along with their inter/intramolecular
interactions in crystals, are elucidated to depict the key factors
for tunable emissions and high emitting efficiency. Furthermore, high-quality
white-light-emitting materials are obtained in various solvents and
polydimethylsiloxane (PDMS) films with combined fluorophores. Overall,
these studies report a promising strategy for the construction of
organic solid materials with color-tunable emission and shed light
on methods for obtaining desirable emission efficiency.
Background: Didymin has been reported to have anti-cancer potential. However, the effect of didymin on liver fibrosis remains illdefined. Methods: Hepatic fibrosis was induced by CCl4 in rats. The effects of didymin on liver pathology and collagen accumulation were observed by hematoxylin-eosin and Masson's trichrome staining, respectively. Serum transaminases activities and collagen-related indicators levels were determined by commercially available kits. Moreover, the effects of didymin on hepatic stellate cell apoptosis and cell cycle were analyzed by flow cytometry. Mitochondrial membrane potential was detected by using rhodamine-123 dye. The expression of Raf kinase inhibitor protein (RKIP) and the phosphorylation of the ERK/MAPK and PI3K/Akt pathways were assessed by Western blot. Results: Didymin significantly ameliorated chronic liver injury and collagen deposition. It strongly inhibited hepatic stellate cells proliferation, induced apoptosis and caused cell cycle arrest in G2/M phase. Moreover, didymin notably attenuated mitochondrial membrane potential, accompanied by release of cytochrome C. Didymin significantly inhibited the ERK/MAPK and PI3K/Akt pathways. The effects of didymin on the collagen accumulation in rats and on the biological behaviors of hepatic stellate cells were largely abolished by the specific RKIP inhibitor locostatin. Conclusion: Didymin alleviates hepatic fibrosis by inhibiting ERK/MAPK and PI3K/Akt pathways via regulation of RKIP expression.
Construction of anti-adhesive polypropylene meshes through the in situ copolymerization grafting of poly(ethylene glycol) methacrylate and dopamine methacrylamide.
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