The single crystal form and uncontrollable topography of CaCO 3 in nature severely restrict its product grade and application. Meanwhile, lignin is still not utilized efficiently. In order to improve this, three types of lignin monomer model compounds as p -coumaric acid (PCA), ferulic acid (FA), and sinapic acid (SA) are employed to induce the growth of CaCO 3 to investigate the relationship between lignin structure and CaCO 3 crystallization. The synthesized PCA and CaCO 3 composite crystals (PC-ACCs), FA and CaCO 3 composite crystals (F-ACCs), and SA and CaCO 3 composite crystals (S-ACCs) are characterized by field emission scanning electron microscope (FESEM), X-ray diffraction (XRD), and Fourier transmission infrared spectroscopy (FTIR) to ascertain their molecular structures and crystal information. The growth rule of the acid and CaCO 3 composite crystals (ACCs) induced by the three units is also explored. The results show that the vaterite and calcite of ACCs can be formed selectively. In the presence of PCA, FA, and SA, pH is the key factor on the phase selection of ACCs. The temperature and organic acid type also play important roles on the formation of CaCO 3 . The ACCs present distinguishing surface topographies at different temperatures. The number of methoxyl in the PCA, FA, and SA decides the phase ratio of vaterite and calcite in the ACCs.
Liver fibrosis is the critical stage in the development of chronic liver disease (CLD), from simple injury to irreversible cirrhosis. Timely detection and intervention of liver fibrosis are crucial for preventing CLD from progressing into a fatal condition. Herein, we developed iron oxide (Fe3O4) nanoparticles (IONPs) and ferulic acid (FA) coencapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs), followed by surface modification with cRGD peptides (cRGD-PLGA/IOFA) for integrin-targeted clinical magnetic resonance imaging (MRI)-traceable treatment of liver fibrosis. The cRGD peptide linked on the surface of the PLGA/IOFA NPs could specifically bind to the overexpressed integrin αvβ3 on activated hepatic stellate cells (HSCs) in the fibrotic liver, enabling the high-sensitive clinical MR imaging (3 T) and precise staging of liver fibrosis. The FA encapsulated in cRGD-PLGA/IOFA showed excellent efficacy in reducing oxidative stress and inhibiting the activation of HSCs through the transforming growth factor-β (TGF-β)/Smad pathway. Notably, the IONPs encapsulated in cRGD-PLGA/IOFA NPs could alleviate liver fibrosis by regulating hepatic macrophages through the NF-κB pathway, lowering the proportion of Ly6Chigh/CD86+, and degrading collagen fibers. The FA and IONPs in the cRGD-PLGA/IOFA produced a synergistic enhancement effect on collagen degradation, which was more effective than the IONPs treatment alone. This study demonstrates that cRGD-PLGA/IOFA NPs could effectively relieve liver fibrosis by acting on macrophages and HSCs and provide a new strategy for the clinical MRI-traceable treatment of liver fibrosis.
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