Hydrophobic Modification on the Surface of SiO2 Nanoparticle: Wettability Control.

Good control of the morphology, particle size, and wettability of silica nanoparticles is of increasing importance to their use in a variety of fields. Here, we propose a strategy to tune the surface wettability of nanosilica by changing the dosage of a chemical modifier. A series of measurements, including scanning electron microscopy (SEM), laser scatting technique, Fourier transform infrared (FTIR) spectroscopy, thermogravimetry, and surface hydroxyl number and water contact angle measurement, were conducted to verify the surface chemistry and wettability of these nanoparticles. Through controlled chemical modification, the contact angle of the treated nanoparticles increases from 34.7 to 155° with increasing amount of dichlorodimethylsilane (DCDMS) within a molar ratio (MR) between DCDMS and nanoparticles of 5.17. The number of hydroxyl groups covered on the particle surface decreases gradually from 1.79 to 0.47, and the surface grafting rate could reach 73.7%. As the addition of dichlorodimethylsilane equals MR 5.17, the contact angle reaches the maximum value of 155°, which displays excellent superhydrophobicity. After surpassing the point of MR 5.17, the contact angle does not increase but starts to decrease, ultimately remaining stable at 135°. It can be concluded that the surface wettability of nano-SiO2 particles can be precisely modulated by varying the amounts of the modifier. Furthermore, the modulating mechanism of the process occurring on the surface of SiO2 particles has been investigated at the molecular level.

P2X7R Blockade Prevents NLRP3 Inflammasome Activation and Pancreatic Fibrosis in a Mouse Model of Chronic Pancreatitis.

OBJECTIVES: The aim of this study was to investigate the role of P2X7R (purinergic 2X7 receptor) and NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome activation in the process of pancreatic fibrosis in a mouse model of chronic pancreatitis (CP). METHODS: Chronic pancreatitis was induced by repeated intraperitoneal injections of 50 µg/kg cerulein for 6 weeks in mice. P2X7R antagonist oxidized ATP (OxATP) or brilliant blue G (BBG) was administered after the last cerulein injection for 2 weeks. Pancreatic chronic inflammation and fibrosis were evaluated by histological score, Sirius red staining, and alpha-smooth muscle actin immunohistochemical staining. We further determined pancreatic P2X7R, NLRP3, and caspase-1 expressions in gene and protein levels and the pancreatic concentrations of caspase-1, interleukin 1ß (IL-1ß), and IL-18. RESULTS: The pancreatic P2X7R, NLRP3, and caspase-1 expressions in gene and protein levels and the pancreatic concentrations of caspase-1, IL-1ß, and IL-18 were all reduced significantly in both the OxATP and BBG groups (P < 0.05). The pancreatic chronic inflammation and the fibrosis indices were all remarkably attenuated (P < 0.05). CONCLUSIONS: P2X7R antagonist OxATP and BBG significantly decreased pancreatic chronic inflammation and fibrosis in a mouse CP model and suggested that blockade of P2X7R-NLRP3 inflammasome signaling pathway may represent a novel therapeutic strategy for CP and its fibrotic process.